Lentiviruses: Me, and you, and Zaboomafoo Part Two!

A few shards and some coordinates, but I have not been able to search with the efficiency I had hoped for. Sorry not to do better - time is too short. Evan Eichler promised his team will look again at candidate CERV1 orthologs.

Whew! Some hot genetics this morning, and I haven't even had my coffee yet! As always, an excellent post for scientist and layman alike.

Abbie,

Forgive me if this seems like an ignorant question, but I'm just an interested layman, so I'm plenty ignorant. :)

You said:

...they didnt even need a complete 'lemur' genomic sequence to figure this out.

If I'm understanding this post correctly, though, even if both genomes were sequenced entirely, it doesn't seem to me that this would be any more of a slam dunk. Would it?

I know it's a lot of work, but I really think you should animated this and present it in more detail at your next debate. This is kinda awesome. And by "kinda," I mean "a lot."

If I'm understanding this post correctly, though, even if both genomes were sequenced entirely, it doesn't seem to me that this would be any more of a slam dunk. Would it?

Nope!

You dont need entire genome sequences to figure out 'where' an ERV is. You just need to know what your surroundings look like :)

OK, but if ERVs are inserted randomly, does that mean that all the individuals that carry an ERV at the same position are descended from one individual?

Abbie,

I am glad you addressed this question, it is one that I have also asked, as you know.

You need to remember that where retroviruses insert in a genome is random. Like Ive said a hundred times before, yes, some like to insert near active genes, and some like quiet genes, but exactly where a retrovirus inserts-- near which active genes, exactly which nucleotides are up/down stream, is random.

Is this random statement an assumption, or a conclusion well backed up by data?

How exactly did you or other scientists determine that the insertion points are random? And are you sure?

Or are random insertion points just a useful model?

For starters, I'd like to see a representational plot of known versus possible insertion points to see if the data used to form the "random" hypothesis is sparse. If the observations are not sparse, you have other hurdles. But I--somebody outside of your field of expertise--suspect the data is sparse. (You wouldn't roll a 1000-sided die 3 times and claim evidence that it is a fair die.)

I am aware that in other disciplines quantization "noise" (error, really) is modeled as a random process, and that this model is useful in many applications, but the fact of the matter is, quantization error is absolutely *not* random. Despite this, and textbook and technical paper authors being very precise in defining the quantization noise as a mere model for quantization error, I have encountered too many university educated individuals who have not paid sufficient attention to this fine point. Quantization error is not random, even if a random mathematical model of quantization error is very often and legitimately used.

A model's usefulness has no bearing on whether or not it is true. Other examples of this fact exist in science and engineering. (As another example, Tycho's sixteenth century geocentric model of the solar system was very useful for constructing navigational charts so that others could accurately sail the world's oceans. But the model's utility didn't make the Earth the center of the solar system.)

He determined that even though the lentiviral ERV sequences were super similar, they are not located in the same genomic regions.

Nice to see you've corrected this to "super similar". During the debate, you had stated that they "determined that they were very different retroviruses".

But a remaining question is, aside from what I presume is a random insertion point model, how do you differentiate between ERVs currently being at different insertion points, and ERVs that have merely been reshuffled. (In this later case, it is actually to the benefit of the common descent hypothesis. But of course, it is a two edged sword--especially if the random insertion point model is not a reflection of reality.)

But a remaining question is, aside from what I presume is a random insertion point model, how do you differentiate between ERVs currently being at different insertion points, and ERVs that have merely been reshuffled.

And Limp Willy proves once again that his reading comprehension is as flaccid as his assets. Did you even read the post?

Kevin,
I'm no fan of WW, but I don't think his point, i.e. how to distinguish between ERVs that are in the same spot bc they were inserted there and those that happened to wind up in the same spot through reshuffling, was addressed in the post. I think the answer is simple parsimony, but i didn't get that from the post.

my question remains, however: if insertion is random, then the only way an entire species can share the same erv in the exact same spot is if that entire species was descended from a single individual who had the erv inserted in that spot. or am I (likely) missing something?

Cool post once again, Abbie! Thanks.

I was wondering if the fact that these 2 endogenizing events happened about the same time means that the lemurs were having an epidemic at that time. Would there be any other evidence of that? Does anything like this virus still infect lemurs?

On another track, if I'm understanding this at all, I would think that while the insertion is at a random point, not all points would lead to a viable lemur, so we wouldn't see them randomly situated in their descendants.

Also, if I'm understanding correctly, I have another analogue. Suppose you're looking at 2 pictures of a house.... they look the same, but you can't tell if they're the same house or just 2 houses made to the same plan. You can tell if you can see the houses on each side, or even if you can just tell how far the neighbours houses are from the one in question. You don't need the actual address (ie complete genome).

dmso74, that is indeed the inference. For why it's simultaneously cool and doesn't violate the principle that populations evolve, check out 'most recent common ancestor' on Wikipedia. Imagine a certain protein that all us humans have a simple gene for. At some point, in all likelihood, it arose in a single individual (sometimes relatively common mutations can happen in separate individuals).

my question remains, however: if insertion is random, then the only way an entire species can share the same erv in the exact same spot is if that entire species was descended from a single individual who had the erv inserted in that spot. or am I (likely) missing something?

Well, of course, Satan could have inserted the ERV's after The Fall to make creationists look like idiots. There is that hypothesis. But apart from that: No, common descent is the only reasonable explanation.

Excellent explanation! I'm sure you'll be referring people to it often.

Shirak,

I can see that happening w a beneficial protein, but why would the individual w an erv have such a huge survival/reproductive advantage?

They don't need one dmso74...Ever heard of genetic drift?

or the founder effect for that matter.

Evolutionary theory isn't all selection any more. There are many other processes that affect change in populations.

"I can see that happening w a beneficial protein, but why would the individual w an erv have such a huge survival/reproductive advantage?"

They don't need one. Most of the content of your genome, indeed most genomes, is selectively neutral.

"Why would an individual w an erv have a huge survival/reproduction advantage?"

I think the clue is in the question. The individual would be one of a subset of that species that survived the epidemic and went on to reproduce more that those that didn't survive.

Also, I think WW was trying to ask the opposite of dmso74. Namely, how could you tell if two species acquired an erv from a common ancestor and then one of the descendant species shuffled the gene to a different place?
His point about the validity of random models with the data ret size was uncharacteristically good, but I'm not sure how relevant it is.

Authors wrote re the multiple Microcebus pSIVfdl copies, 'They could result from repeated germline insertions of the same or very similar circulating lentiviruses, intragenomic retrotransposition events, reinfection by an endogenized copy, or a mix of these mechanisms.' WW has a point which the authors don't feel able to refute entirely, so why then is Abbie being dogmatic that they result from descent? (as opposed to the well demonstrated and distinct endogenisation in Cheirogaleus). Paradigm blinkers again?

jon and eddie,

thanks for your thoughts. your two answers work really well together and gave me a duh! moment.. the population gets cut down to just a few individuals thanks to the virus.. then founder effect can take over from there.. could help explain why the speciation event took place as well (founder effect).. neat!

One common and well founded answer to the question about advantage of ERVs is protection against XRVs (near identical exoviruses)- well studied in the case of JSRV and eJSRV. (A Paradigm for VirusâHost Coevolution: Sequential Counter-Adaptations between Endogenous and Exogenous Retroviruses Nov 2007. PLOS)

cprs/charles-- Hi! Glad you made it over to the new ERV. As Im sure you have noticed, your appearance at old ERV was simply bad timing, as I am currently dealing with a Creationist named Charles who doesnt understand ERVs with an obsession with the word 'paradigm'.

Unfortunately, second Charles Creationist, you dont appear to understand ERVs any more than the first one.

Authors wrote re the multiple Microcebus pSIVfdl copies, 'They could result from repeated germline insertions of the same or very similar circulating lentiviruses, intragenomic retrotransposition events, reinfection by an endogenized copy, or a mix of these mechanisms.' WW has a point which the authors don't feel able to refute entirely, so why then is Abbie being dogmatic that they result from descent? (as opposed to the well demonstrated and distinct endogenisation in Cheirogaleus)

There is more than one copy of this lentiviral ERV in the genus Microcebus. Say there are 30 insertion sites-- these 30 could be the 'result from repeated germline insertions of the same or very similar circulating lentiviruses, intragenomic retrotransposition events, reinfection by an endogenized copy, or a mix of these mechanisms'. The authors of this paper didnt give a shit, because its irrelevant to the goals of this paper-- two independent events in two genera, or common descent?

Lets say there are 30 copies of this ERV due to a mix of all of those listed mechanisms.

That doesnt change the fact that these insertions are orthologous between Microcebus species. Read the next paragraph of the paper.

We see this in the human genome HERV-K family. Many members of this family are not independent infectious events. They are the result of a HERV-K reverse transcribing and plopping back into the same genome.

One common and well founded answer to the question about advantage of ERVs is protection against XRVs (near identical exoviruses)- well studied in the case of JSRV and eJSRV.

Creationist Claim #6a. Great job!

Now go read about MMTV for a counter example-- endogenous MMTV leads to increased susceptibility to exogenous MMTV, and actually decrease survival rates after infection with some kinds of bacteria.

Though ERV proteins are occasionally (read: rarely) beneficial, ERVs are not present in genomes because they are beneficial. They are present because of random genetic drift, and because there is no way to get rid of them outside of the recombination event I stated in this post, which still leaves solo LTR footprints.

Does everyone who comments here know that the douchebag who commented in the middle of part 7 of the "debate" video is Rhology? I mean, his idiocy in that video is unmatched by any of his comments I've ever read here.

dmso74, your hypothetical pandemic situation isn't required. Like jon said, think of genetic drift, which can be huuuuuuuge. First, consider that insertions can happen all the time in various places. Let's consider just those that are neutral, which are going to have a lot of potential insertion areas w/ big free-living eukaryotes like lemurs (introns, etc). Now, the foundering effect would certainly increase the chances of a single mutation being passed on entirely via drift, but it isn't required, as these things, again, happen very often on an evolutionary timescale. So we look at this one mutation and compare it to the rest of the population: they don't have the insertion. But, since there's no selection happening, there's nothing really stopping it from taking hold in the population and there are many simulations of how this stuff works, essentially taking a drunkard's walk.

Allopatric speciations events and all that also make it interesting. Let's say 12% of the population has this random, non-selected mutation hundreds of years later and *then* a small group of 100 finds its way to a separate location and the groups become isolated. Only it wasn't a completely even sampling: by random chance, 40% of the founders have this ERV. That's a foundering effect that had nothing to do with the actual disease but still let this ERV's frequency in the population go way up!

WW

But I--somebody outside of your field of expertise--suspect the data is sparse.

Oh for fuck's sake. HOW LONG HAVE YOU BEEN READING THIS BLOG? You don't recall reading about any other retroviruses that have been found in genomes? Little tidbits like there are about 98,000 ERVs in the human genome alone? Other tidbits like we can *experimentally* map insertion sites?

If we are talking about lentivirus insertion sites only, there the data indeed is sparser, which was clearly mentioned in the post, and if you had read and understood it you would not need to "suspect", you cretin!

So, do you think that because there's less data on lentiviruses, it's reasonable to suspect that they, unlike other retroviruses, are somehow are able to home in to the exact same location out of billions of nucleotides in the host genome? Until we find a lentivirus with a little fairy or computer inside it, HOW ABOUT NO!

I am aware that in other disciplines quantization "noise" (error, really) is modeled as a random process

What the fuck does quantization error have to do with the distribution of insertion sites in a genome?

William, there's a fair bit of evidence that ERV insertions will be more or less random (stochastic might be more accurate than random). In particular, retroviruses themselves insert at pretty close to random points. This can be observed in the lab.

Lemurs are cool. That is all.

OK, but if ERVs are inserted randomly, does that mean that all the individuals that carry an ERV at the same position are descended from one individual?

I think the correct statement is that it's highly likely that they both share a common ancestor that had that particular insertion.

However, since the insertion points are random, it is possible that, just by chance, two independent insertion events could lead to the exact same insertion of nearly identical viruses in the same location. With all of the tens of thousands of viruses in our genomes and other genomes, it stands to reason that eventually we'll find one or two such chance insertions.

Similarly, there is a convoluted sequence of events which can cause a phantom of no common descent where there actually was common descent. That is, imagine if the original common ancestor had a duplicate of the region where the ERV was inserted: one block of DNA with the ERV, one block without. Furthermore, the ERV itself might have inserted itself into more than one location, either originally, or due to copying itself elsewhere in the genome. So, again, this sequence of events is highly unlikely, but just given the large sample size, chances are we'll see it happen once or twice.

Therefore, these ERV measures can show to a very high degree of precision whether or not a specific insertion is or is not homologous. But I think more work is required if you're not content with merely ballpark one-in-a-million odds of being correct.

Typo: Oops, meant ballpark one-in-a-million odds of being incorrect. Not the other way around.

Jason Dick,

The problem with your argument is that the ERV evidence for common descent is not just that there are common insertions between two species. It's that there is a pattern of insertions between multiple species, even crossing different genera, that is exactly as predicted by common descent. The odds of such a pattern arising by chance is for all intents and purposes impossible. If what you were saying was true, then we would expect to see some ERV's in common between humans and, say, chimps, organgutans, gorillas, rodents, etc. But the specific ERV's would be different between each pair (No reason we would share the same ERV's with chimps as gorillas, nor any reason that chimps and gorillas would share the same ERV's that they do with us.) And rodents would share a portion of ERV's with us in proportion to their genetic similariy to us, not in a pattern that allows the creation of a phylogenetic tree based on ERV evidence alone. The last point is an important one. ERV's can be used to contruct phylogenetic trees which, by itself, is evidence against coincidental separate insertions. And the capper is that these trees are consistent with those based on independent evidence from, say, the fossil record and other molecular genetic evidence.

SHirak et al.

My (perhaps mistaken) understanding is that specific ERVs are fixed (everyone has them) in a population at the same spot in the genome, implying that they came from a single insertion event in a single individual. is there any consensus on this issue?

Excellent post!! Thanks, Abbie!

And thanks "Shrunk" for the last comment (#29). The sum-up...

ERV's can be used to construct phylogenetic trees which, by itself, is evidence against coincidental separate insertions. And the capper is that these trees are consistent with those based on independent evidence from, say, the fossil record and other molecular genetic evidence.

...will be so useful in creation smackdown. I've been lurking here for a few weeks, and this post and comment are my best take-aways thus far.

Thanks Joshua Zelinsky. Can you reference a paper (preferably available freely to the general public) that proves this, or even just provides very strong evidence, and doesn't just assume it?

Abbie is silent so far, perhaps because she doesn't want to get pinned down on this point so critical to her argument.

So, Abbie, do you think that the fact that the Martin et al paper, Retroviral DNA Integration: ASLV, HIV, MLV Show Distinct Target Site Preferences is sufficient to prove your assertion that these are random? Its figure 1 *looks* random, after all. Is "looking random" sufficient to demonstrate randomness in your scientific opinion?

Or is there another paper you can cite to scientifically justify your assertion, "You need to remember that where retroviruses insert in a genome is random."?

Or should we just take it on faith, and not fact check your assertions?

Oh my fucking god do you know how to search at ScieneBlogs, WW? Do I need to ask teh management to create a video tutorial to teach idiot Creationists how to use teh Google Machine?

I addressed that paper a year and a half ago, genio. Way to stay on the ball, there.

I know you addressed the paper, which is why I brought it up. I am asking you to clarify if you think that a picture with lolipops that appear to be randomly dispersed is sufficient to back up your claim, in your mind, that integration points are random?

If so, I will spend a bit of time educating you and those who might be misled by your conclusion that random looking data isn't very good evidence of a stochastic process. (Indeed, the authors of that paper don't seem to draw the conclusion you do from figure 1.)

If not, I'd rather you just cite a paper that backs up your claim. Or is the "random" claim, mentioned in your argument, not actually a key point of your argument?

I'm not sure what point you think you have here, Mr. Wallace. You're trying to claim that ERV's keep showing up in the exact same location, not only in every single member of a species but in different species, not because of anything to do with inheritance, but because retroviruses insert into only a few preferred sites in the genome. So all you have to do is cite some evidence that retroviruses do just that. In the paper you are discussing, for instance, there should be many insertions that are identical if you are correct. But, no, every single one of the over 3000 insertions is in a different, unique locus. None of your fancy talk about "quantization error" can hide the fact that can't point to a single instance of a retrovirus inserting into the same point of a genome on two separate instances. Unless you know of such an instance?

William, why don't you read Abbie's earlier discussion of the papers in question or just read the paper you cited. That paper is quite clear that insertion is randomized process with some retroviruses having slight preferences for certain regions.

Moreover, fixed insertion points wouldn't give you a nested hierarchy based on ERVs. This should be obvious if you spend about 30 seconds thinking about it.

"With all of the tens of thousands of viruses in our genomes and other genomes, it satands to reason that eventually we'll find one or two such chance insertions."

Well, no actually. There are 3,000,000,000 base pairs in the human genome. Therefore the chance that two separate events happen at then same base pair is 1/3,000,000,000 (Pick one base pair at random, what are the chances of picking that base pair again?). Now, if we have 5,000 infections in pairs (so that there are only two of each kind of insertion in the genome), We have only 5,000 chances to hit an event with odds of 1/3,000,000,000 and we have approximately 8 in a 1000 chance of getting one coincidence.

Now, if we cannot tell any of the retro-viral insertions apart from each other the odds go up very significantly to approximately 4 in 10.

But there are two points to remember: as Abbie pointed out, we can tell the ERV's apart from each other, so the actual odds are better represented by the first calculation, and, more importantly, we have not actually checked every one of those 10,000 ERVs, but have only checked the best ERVs, and finally, we haven't gotten just a single match, but have gotten, what 12?

Even going off the second calculation I suspect the chances of getting that many hits are very very slight (I can't think of how to due the calculation just yet, check out http://en.wikipedia.org/wiki/Birthday_paradox for to try it your-self, could you just use a normal approximation?)

First, the important question, and the only claim I have made so far, is that the random appearance of data doesn't establish that it is random. It could be random, but, especially in the case of sparse data, there could be latent relationship.

I will spend some time illustrating the shaky ground she's on, if Abbie confirms that the random appearance illustrated in figure 1 is the basis of her claim.

Nice goal post shift attempt, Skunk.

We're talking about Abbie's claim. "We need to remember...".

By "remember" does she mean "take on faith" or does she mean that there is a study that establishes once and for all that the integration points are stochastic?

Joshua, I did read the discussion. Where do you think I found the paper. I'll quote Abbie:

Look at Figure 1: All those blue lollipops are places they found where HIV inserted itself.[Figure 1 ommitted]...Theres a lot more than one lollipop in that figure.

Is this the best evidence she has? Appearance in a graph? Note she has still not confirmed it, because, I suspect, she knows this straw man of data appearing random as strong evidence of a stochastic process is easily slain as very weak evidence.

Joshua, the opposite of random isn't "easily predicted", or even "fixed". I'm not pointing this out for your sake, because I suspect you know this. But for the sake of others, and for the sake of clarity.

That paper is quite clear that insertion is randomized process with some retroviruses having slight preferences for certain regions.

My understanding is that comparison datasets were selected randomly to remove bias, but my reading of the paper is that it concludes that a bias was detected. This bias was not completely characterized, just reported. The bias rules out a rectangular PDF, but doesn't authoritatively characterize the distribution of ERV integration, does it?

And even if it did, the analysis of a mere 3,127 integration sites is not prima facie evidence that ERV insertion is a stochastic process. Indeed, I didn't find in the paper a description of the criteria used to select the 3,127 integration sites. Was every known integration site examined? Were duplicates removed? Could duplicates even be identified? Are the 3,127 integration sites claimed to be ergodic?

So, once again, slaves to evidence though some of us claim to be, the request for evidence that ERV insertion points are random remains glaringly unanswered. If the insertion points are random, so be it. I don't know. But convince me scientifically, don't just tell me that I "need to remember". I am not a chance worshiper, who falls for the "stochastic process of the gaps" argument, but neither do I deny that chance happens.

The question is, are ERV integration points stochastic, and what paper or papers, preferably publicly available, have settled this question once and for all?

Assumptions aren't bad, as one of Abbie's least favorite teachers recently pointed out, but you should be aware of them, disclose them, and be aware of the risks involved in basing conclusions on them.

Shrunk: "So all you have to do is cite some evidence that retroviruses do just that. In the paper you are discussing, for instance, there should be many insertions that are identical if you
are correct."

As a general policy I would like people to simply ignore W.W. since it is highly improbable that he will say anything important, but I will use the shenanigans to launch into scientific philosophy.

You make an excellent point and I would like to make it explicit why the burden of proof is on W.W. to show that retro viral insertion is not random, and not on Abbie to show that it is.

Proving that something is random is essentially impossible, and to attempt to do so is non-scientific*. Why? Saying that something is random is equivalent to making the claim 'there is no pattern which can explain these data.' A moments reflection will tell you why this cannot be proven. The assumption that data has no pattern is generally the null hypothesis. We simply assume that the data is random until we have reason to think otherwise.

A passing familiarity with cryptography will serve to illustrate the point. It is very easy to see that a stream of data contains an encrypted message once the message has been decoded (For instance do you believe that this post is just a steam of random letters that just happened to cary meaning by chance?) however, it is actually impossible to be sure that a stream of data does not contain an encrypted message. A 'one time pad' encryption is impossible to crack http://en.wikipedia.org/wiki/One-time_pad, so you can never be sure that a message wasn't encrypted using this method.

I could go on to address W.W. nonsense specifically, however, the broader philosophical issue was the only part that interested me.

Just my two statistically significant cents.

*This isn't absolutely true, just a useful heuristic.

WW accidentally impinges on something slightly relevant to the topic that he's trying to address, and that regards the actual randomness of inserted ERVs.

The positions that we see historic ERV insertions in segments of an animal population are not going to be perfectly random. There will undoubtedly be slight biases due to the accessibility of the virus to particular partions of the genome. So it's almost certainly not a perfectly uniform distribution that we'll see ERV insertion; it will be biased by the infected cells' use of their DNA and probably the particular methods the ERVs use to insert themselves.

Secondly, there will also be a substantial bias away from various parts of the genome: insertion into any critical part of the genome will prevent the organism or an infected germ cell from producing viable offspring.

So, yes there are biases in the location of ERVs in the genomes. No, they don't affect the validity or results of the study -- there are still huge numbers of potential insertion sites.

While Matthew Akerman is correct when it comes to analysis of data encrypted with a one-time pad, anybody familiar with Johnson noise, Brownian motion, or quantum mechanics can tell he is engaging in sophistry. Consider this: one-time pads cannot exist without a source of randomness. Somebody get a fire extinguisher in here--another straw man just went up in flames.

dmso74, you got it. Even with reshuffling, the chances of it reshuffling to that *exact* spot on the genome are pretty low, so it's a good inference that common ancestry is responsible for those shared ERVs.

WW, even if there's a latent pattern (which you are concocting in your head), the data points to the insertions being all over the place, indicating a large amount of effective randomness. Take your own example of Brownian motion: there's a lot of randomness in there, even if trends can be identified, and it is a stochastic process. For something even more complicated, there's random walks, which again illustrate this randomness.

No one asserts that they have absolute knowledge of a process being random, and that's what someone would need to avoid your silly tangential claim: 'it could still have a trend of explanation!'. Instead, we look at the actual data and see what patterns there are. So far, it sure looks like insertions can happen all over the place and unless you'd like to point out a strong correlation, you can STFU and go read a book.

Thanks for the explanation, Matthew Akermann. I agree, it's pointless to expect anything but nonsense from an evolution-denier. Still, it's fun to push them to see just how ridiculous their arguments will become.

If I understand you correctly, we can never say a pattern is random because we can never be certain that a non-random pattern exists that would be evident if we had a larger data sample. For instance, suppose we have a series of a million digits that continually repeat in the same pattern, but otherwise have no fixed relationship between each other. If we were to analyse those digits over two or three repetitions of the cycle, we would be able to discern the pattern. However, if we stopped anwhere before the millionth digit, the series would appear completely random. Is that kind of that you're saying?

In this specific example, since AFAIK we have no documented examples of retroviruses independently inserting into identical sites, there is no possibility of determining that there is preference to particular loci. However, and this is where I begin to get way out of my depth, it may be possible to determine what kind of selectivity is necessary to support Mr. Wallace's belief. Remember, what he is claiming is that retroviruses are so picky about where they insert that ERV's have independently arisen in the exact same location, down to the precise base pair, in every single human, chimpanzee, gorilla. orangutan, and many species of monkey. And that this is not due to inheritance, but to a large number of identical insertions. Even the ERV's fixed within a single species would not have resulted from common descent (if you are denying common descent as an explanation for interspecific common ERV's, then I don't see why you would accept it for intraspecific ones.)

Now it seems to me it should be possible to estimate what degree of specificity of retroviral insertions we should observe in order to produce this result. Mr. Wallace says 3000 insertions is too small a sample, but I wonder how he knows this? He says he bases his claims on evidence, but has yet to produce any for his "picky retrovirus" hypothesis. My gut feeling is that this degree of specificity should be readily observable in real time i.e. we should be finding retroviruses uncannily always appearing at the same limited number of points in the genome when we analyze new infections. (It's worth noting such a finding would be of great practical importance, as it would provide a potential mechanism for precisely directing genetic therapies.) But as I say, that's just intuition on my part. Surely Mr. Wallace or some other "creation scientist" would be able to mathematically determine the degree of specificity we should be observing. Of course, this would only be able to falsify, and not confirm his hypothesis (i.e. if it turns out that, in the number of insertions we have documented, identical insertions should have been observed, and they haven't been, then the hypothesis is disproven. If it turns out we don't yet have enough observed insertions to rule out the hypothesis, it still doesn't mean it is true). However, since creationists claim to be real scientists, that shouldn't deter them.

How about it, William Wallace?

"If I understand you correctly, we can never say a pattern is random because we can never be certain that a non-random pattern exists that would be evident if we had a larger data sample."

Actually, that is not what I am saying. I am saying: When we say that a pattern is random, we are under no obligation to provide rigorous scientific proof of this assertion. If someone else believes the pattern to be non-random, then they must demonstrate how it is non-random. A belief that it is random is our default position until we have some reason to think otherwise.

As for the second part of your post, it is part of a discussion with W.W., and consequently I will have to ignore it. ;)

I don't know why you are allowing WW to derail this thread into a conversation about whether or not the insertions are random. That may be an interesting mathematical discussion, but the evolutionary significance of these insertions is in relation to common descent. The SITE of the insertions in the genome can be used to detect the difference between insertions inherited from a common ancestor and independent insertions in different organisms in a lineage.

Common descent is the only rational explanation for the many insertions that are found in the genomes of humans and chimps, since the sites of the insertions are identical. It doesn't matter if they are random or not; the identity of the sites is the important parameter. The work discussed by Abbie above removes another weak apologetic argument (i.e., maybe they were inserted independently in chimps and humans, how would you know if that was the case?). We can tell the difference. And chimps and humans still have a common ancestor, one proof of which is the number of insertions at common sites in the genome.

So, WW, how about paying attention to the real issue? What explanation do you have now for the common insertions at homologous sites in the genomes of chimps and humans?

Matthew (#45):

I think we're really saying the same thing. My point is that to say something is non-random is an unfalsifiable position. If there is no evidence of a non-random pattern, the creationists could always say, "You need a larger sample" and they could continue to do this ad infinitum. At some point, however, it is possible to say, "Even if we did find some evidence for preference of particular sites by using a larger sample, at this point we can say that any such preference must be too weak to explain universal fixation of these ERV's without resorting to common descent as an explanation." My question to WW (you can stop reading here, Matthew) is why don't creationists try to define the sample size at which that statement can be made, thereby formulating a falsifiable hypothesis that would allow creationism to be dismissed, by creationists' own criteria, once and for all? That's what any real scientist would endeavour to do.

@Shrunk:

Because they like it that way. They simply can't win without the use of a grab bag of logical fallacies.

This randomness thing looks like a mixture of moving the goalposts and pointing at perceived "gaps" to me. No matter how large the sample size gets, they'll always say, "well it just isn't big enough yet!" and deny the research. Then they'll claim that this is evidence for the situation being non-random when, in fact, it isn't at all.

#21 Sorry to reply so late, but I'm well out of sync with OK and busy. Thanks too for your patience in answering someone you clearly regard as troublesome.

I don't profess expertise in ERVs, but I do profess fascination, and I envy your opportunity to study something so intriguing - ERVs necessitate major paradigm shifts from classical genetics and standard epigenetics whatever one's prior assumptions, especially given the intricate functional ties between ERV genes and LTRs and host genes and inducers.

The question you posed here, Abbie, is seminal, 'How do you tell the difference between an ERV that is shared because of common descent, and one endogenized independently in two species?' By claiming all the Microcebus insertions are orthologues either you are presuming what the authors do not or you're using a different definition of orthologous than I am used to (homologous genes from a common ancestor). My assertion stands - are you not being dogmatic without proper grounds? I am not at all convinced that the paper answers your question neatly - not yet anyway.

Who claims defence against XRVs, specifically JLR (JSRV late restriction), is universal? What's interesting is that the inactivating mutation is apparently not random - so suggest the authors - ('the R21W substitution is not strictly necessary for JLR, as single JSRV mutants carrying amino acid residues other than R at position 21 are incompetent for viral release and transdominant over JSRV')- they also hint at host exploitation of endogenisation (http://jvi.asm.org/cgi/reprint/81/4/1762) - the MMTV counterexample is interesting but it's not so surprising to see ERVs facilitating as opposed to blocking XRVs.

By the way, when you claim ERVs are rarely beneficial what do you make of the Atlanta group's claims that 51,197 ERV-derived promoters intiate transcription in man, including 114 start sites which are responsible for 97 genes (Bioinformatics 2008.21.12.1563-67)?

Best wishes, keep up the blog - even though your subtitle is blasphemous and does you no credit. I'll be following even if I don't reply again.

Orthologous applies to host genome position not ERV origin, I understand better, and should have read your reply more carefully.

Shrunk, you're a very dishonest person. Your claimed summary of my arguments is not an accurate reflection of my arguments. Matthew Ackerman has already pointed out that you did not summarize his argument accurately, either, so you're getting it from both sides.

To address the point about randomness, you can see in #5 that I am asking for evidence, good evidence, not proof. Evidence of randomness can come in a variety of forms, from weak, to strong.

The reason I am asking for this is because Abbie based her argument on the random assumption. If you look at #38, I said it is okay to have assumptions, but the argument should be properly stated. What Abbie is really arguing, it seems to me, and you're welcome to correct this if I am wrong, is ~"Based on the assumption and preliminary data that ERV integration loci is random variable, and the assumption that, once integrated, ERV sequences do not get reshuffled intact, we can differentiate between quasi-contemporaneous ERV integrations in different species from ERV integrations that were inherited from a common ancestor infected once."

For instance, suppose we have a series of a million digits that continually repeat in the same pattern, but otherwise have no fixed relationship between each other. If we were to analyse those digits over two or three repetitions of the cycle, we would be able to discern the pattern. However, if we stopped anywhere before the millionth digit, the series would appear completely random.

Shrunk, this example is valid, with some additional clarification that I won't delve into. There are interesting counter examples, as well. If you consider quantization error modeled as noise, for example--if you analyze an ergodic ensemble of real valued continuous time signals against their quantized discrete time counterparts, you will see that quantization errors have the characteristics of random noise. However, if you take a specific instance of a real time signal compared to its sampled and quantized counterpart, and analyze its quantization error, it will not be noisy at all. The quantization error will not only be deterministic, it will be periodic for a periodic input signal. So, in this counter example, less data--in the way of a single signal--shows a readily discernible and deterministic pattern. Whereas more data--in the way of an ensemble of ergodic signals--shows a pattern of quantization error having the characteristics of a random variable, hence the useful quantization noise model.

[#46]I don't know why you are allowing WW to derail this thread into a conversation about whether or not the insertions are random.

Simple. It is not derailing. Abbie in the OP said that we need to remember that insertion locations are random. The point is critical to her argument, and stated by Abbie as though the matter is settled.

What explanation do you have now for the common insertions at homologous sites in the genomes of chimps and humans?

Are you suggesting in effect that only a restaurant owner can be a restaurant critic?

I'm just trying to evaluate the strength and weakness of Abbie's argument.

William whether the process is random, statistically random, or stochastic doesn't make any difference. The analysis functions fine.

We can see modern retroviruses (such as HIV) insert themsleves into many different spots so we know that retroviral insertion. So there's strong evidence that the insertion positions are more or less statistically random.

And again there's the basic issue you seem to be missing: If there were ordered, highly preferred insertion points then we wouldn't see a nested hierarchy. Saying something like "well maybe the ERVs insertions are non-random" doesn't even deal with the matter.

Limp Willy: the master of the "Have you quit beating your wife yet" question. He does nothing but lie, obfuscate, and ignore any evidence that contradicts his narrow worldview. Then he somehow pretends that he is "just asking".

How about it, Limp Willy? Quit beating your wife yet?

To WW,

I don't know how I've been dishonest in simply reiterating the fact that it's not up to us to prove that retroviral insertion is random. Again, simply providing an example of two independent yet identical retroiral insertions is what's required for you to at least have a basis for starting the discussion. That by itself won't be evidence for non-random insertion, of course. But without that you don't even have the barest basis to even start considering this as a valid hypothesis, no matter how much impressive-sounding gobbledygook you can manage to type about "quantization error" and "ergodic ensemble". Are we supposed to be impressed by that? Sorry, not.

When I asked What explanation do you have now for the common insertions at homologous sites in the genomes of chimps and humans?

WW weaseled: Are you suggesting in effect that only a restaurant owner can be a restaurant critic?

No. I'm suggesting that by concentrating solely on a definition of randomness, you are avoiding the critical point made by Abbie in the OP. And, unsurprisingly, you are still avoiding it. So I'll ask again, politely.

What explanation do you have now for the common insertions at homologous sites in the genomes of chimps and humans?

It's very simple, William Wallace. So simple that you should be lobbing those accusations of dishonesty at yourself.

WW said:
"To address the point about randomness, you can see in #5 that I am asking for evidence, good evidence, not proof."

A distribution with relatively similar frequencies throughout the gnome. You know, like what we have. Like others have said before, however, the null hypothesis is that there isn't a general pattern: that is, you have you posit and show that one exists, which is reasonable given even diffuse data. Additionally, if new data coming in showed a correlation, you'd *still* have to deal with the data we have showing that ERVs exist and are inserted into relatively inactive areas.

I hope this won't be redundant to everyone here, but I thought I'd offer this explanation for why the observed pattern of ERV insertions is considered irrefutable evidence of common descent.

Let's imagine we have a board containing 3 billion slots representing the human genome (each slot a base pair). We also have a bag containing 90,000 marbles, each representing one of the ERV's contained in that genome. Each time we pull a marble out of the bag, we then reach into another bag that contains 50 million different marbles, each denoting a specific slot on the genome-board (50 million being the minimum number of available sites available for a retrovirus to insert). Once we have pulled a marble out of the second bag, we then but the first (ERV) marble into the appropriate slot on the board.

Now lets suppose we perform this task with a human, a gorilla, a orangutan and a chimpanzee, each pulling marbles and placing them on the board in the procedure described above. Obviously, the task will take a rather long time, but at the end we look at each primate's board to see how many marbles have been placed in the same slots. Now suppose you find that each board has 12 of the marbles in exactly the same place, and there are no other marbles in common between any two boards. Would you be surprised? So surprised that you would in fact be certain that something else must have explained this besides random chance?

There's more. Because ERV's contain a matching pair of LTR sequences which are subject to random mutation, an ERV can function as a molecular clock to allow estimation of the time of insertion. As it turns out, this method confirms that the common ERV's have been inserted at the same time. So, in our game, this would mean that those twelve marbles were not only placed in the same slot for all for primates, but they were drawn from the bag at the same time in all four instances. I'll let the more mathematically inclined calculate the odds of this happening by chance, but I strongly suspect it is somewhere between, "Yeah, right!" and "As if!"

Yet even this is an underestimate of the unlikelihood of what we actually observe. It's easy to forget the reason such a big deal has been made over ERV's. It's true that they provide strong evidence for common descent, but everyone who's not a faith-addled creotard already knew common descent was real. What was exciting about the finding was that they provided a tool to create phylogenetic trees as a means of confirming or clarifiying phylogenetic relationships based on other paleontological and molecular evidence. So even my analogy, complicated as it is, is oversimplified. A more accurate one would be if we had predicted a specific pattern of common ERV marbles (more in common between chimps and humans than between humans and the other two) and ended up with that exact pattern.

Hope that helps more than it confuses....

D'ja ever notice how creationists invoke probability when arguing against evolution in general, but then when faced with ERVs the factor of probability goes right out the window? Keep on keepin' on, guys!

Shrunk, you're a very dishonest person.

Posted by: William Wallace | April 10, 2009 12:31 PM

IRONY was found dead on the popular science blog ERV on the afternoon of April 10, 2009. Funeral services will be held on Saturday, April 11, 2009 at 2:00 p.m. The bereaved ask that you send donations to NCSE in lieu of flowers.

D'ja ever notice how creationists invoke probability when arguing against evolution in general, but then when faced with ERVs the factor of probability goes right out the window? Keep on keepin' on, guys!

That's because they have bigger probabilities. They take their probabilities and, like, multiply them together and stuff. You ain't seen probabilities until you've seen a creationist probability.

And like the lying weasel he is, Limp Willy *always* runs away when confronted with his lies.

Come on, big man. Answer the damn questions! You're so smart and edumacated, and you can't answer simple questions? One might almost start to consider that you don't really know anything at all!

I suppose you believe the retort that any phenomena not fully understood can be attributed to chance, and the burden of proof is *not* on the one asserting that it is chance, but on the skeptic seeking a scientific justification for the assertion.

If you believe the forgoing is a fair representation of the argument you believe has not been addressed, cut and paste the preceding paragraph into vi (I understand there are some software engineers here), and then issue the command

:%s/chance/God/g

Then, read again, let me know what you think.

And note, "slave to evidence" Abbie has not yet addressed the point first brought up in [#5].

Some of these ad hominems against WW are themselves very damning for their authors: they reveal intellectual impotence, immaturity or both. There are real issues here let them be addressed.

cprs - they are not real issues - this is garbage willie keeps throwing against the wall. Then, when it doesnt stick, willie keeps pointing to the spot it fell from and saying, why wont y'all tell me what keeps that garbage there on the wall. At a certain point, it gets tiresome to keep pointing out that the crap didn't stick, and there is no garbage on the wall.

The issues have been dealt with, ad nauseum. His central issue has been dealt with here, quite well. Willie keeps hammering it nonetheless.

People insult him, because they are tired of responding to his crap over and over and over and over and over and over and over and over and over.....

@cprs #63:

On the contrary, they simply reveal that we're sick of WW's constant obfuscation, snotty attitude, and deplorable reading comprehension skills.

He's like a child who has learned a few big words and gets a kick out of playing the "I'm not touching you I'm not touching you I'm not touching you I'm not touching you I'm not touching you I'm not touching you" game.

It's like trying to have an honest conversation with a first-year Philosophy student: boring, infuriating, and ultimately pointless.

WW has demonstrated no reasonable desire to have an actual conversation: he seems interested only in throwing what wrenches he can into the machinery and claiming they slipped when caught red-handed.

In the digression caused by WW's desparate "non-randomness" argument, I think an important point has been lost: Charles Jackson presented the lemur study as a refutation of the ERV evidence for common descent, but there is no way anyone who understands the paper could make that claim. So the options are 1) Jackson cites papers in his talks that he does not even understand; 2) Jackson does not even understand the ERV evidence for common descent even though he claims to be competent to debate on the topic of molecular evidence for evolution; 3) Jackson does understand the paper and the evidence, but intentionally misrepresents them on the assumption that his audience will be sufficiently ignorant not to realize he is doing so. If (3), then it is clear his assumption is correct, for the creationist part of the audience, that is; the video clip linked in Abbie's post was actually put up by a creationist, oblivious to the fact that this was a major gaffe by their man.

If you've read the comments on the debate itself, you'll know that I sent Jackson an email to clarify whether he actually understands the ERV evidence, but all he responded with was a request for another debate. I'm not sure if he thought I was connected with Abbie in some way. Weird.

cprs: "Some of these ad hominems against WW are themselves very damning for their authors: they reveal intellectual impotence, immaturity or both. There are real issues here let them be addressed."

If your idea of 'intellectual impotence' and immaturity is using insulting language with a trolling, lying idiot, I think you have some growing up to do yourself. If you don't like negative verbiage on the internet, you can ignore it like mature individuals.

If you're referring to ad-hom as an actual fallacy, then it's again to be expected when the individual is *actually* a trolling, lying idiot. You'll notice he's largely ignored the direct responses to his inanity. This is because he's also a coward. I have to wonder how long you would entertain someone so obviously dishonest. Presumably for weeks, given your clear moral superiority.

Shirakawasuna's challenge: Shirakawasuna, why don't you document some of my supposed lies.

Optimus Primate and Lee, Abbie made an assertion, but she hasn't offered a citation to a paper published in a peer reviewed scientific journal that concludes, and not just assumes, that the insertion points are random. I had to search on my own, and the best I could find was her claiming that integration points are random because figure 1 of some paper (that shows a bias) has no pattern she can discern.

Other than variants of "yes this is true, erv insertions are random" I haven't ignoreed much on this thread at all.

Indeed, I am dammned if I do, dammned if I don't. If I respond, I am a troll, but if I don't, I am a coward [#61].

It seems that the trolls here are the ones who are not addressing the issue at hand, but instead resorting to the types of responses you'd expect to see on a Jerry Springer show. Give a journal citation, show the evidence, reframe the argument, or admit that it is based on an assumption without strong scientific evidence.

"#68
Shirakawasuna's challenge: Shirakawasuna, why don't you document some of my supposed lies."

How about you take my *actual* challenge and reply to the many and various points that refute your whining?

By not doing so and acting like you have, you prove the dishonesty.

WW: I had to search on my own, and the best I could find was her claiming that integration points are random because figure 1 of some paper (that shows a bias) has no pattern she can discern.

And in this search of yours, did you uncover any evidence for non-random insertion that we've been asking you for since this thread began, and which you have yet to provide?

Perhaps you could explain how we would discern preference for a specific site when we have 3127 retroviral insertions with no duplication between any of them. Do we give each virus a survey form to rate how much they like the particular site they landed in? If you do decide to go against form and actually answer this question, please do so with relying on obscurantist jargon.

On a side note, it's interesting to note that WW is essentially admitting that his belief in creationism now rests on the barest thread: The hope that retroviruses possess some mysterious ability to guide themselves to specific points in the genome. No evidence for this, of course, but he's convinced that it must exist somewhere. He has no choice, really. The only alternative is to accept the reality of common descent.

WW speaks the truth: It seems that the trolls here are the ones who are not addressing the issue at hand

Unfortunately he is the troll, under this definition and many others. Twice now he has ignored this question, which is central to the points raised in the OP. Will WW whiff again on the third attempt? Let's find out.

WW, what explanation do you have now for the common insertions at homologous sites in the genomes of chimps and humans?

WW:

Here's the thing: why shouldn't insertion points be random? Viruses are like bad dates -- they shoot and leave. They have no mechanism to make sure where in the genome their DNA actually winds up; barring an assertion of some kind of cellular channel that specifically channels foreign DNA to a specific dumping spot (something that I don't think there's any evidence for), the burden of proof is on someone who asserts that it isn't random.

Frankly, you sound like Dilbert's boss being outraged at finding out that 40% of all sick days are taken on Monday and Friday.

It's even worse for little Willy. All we need is _one_ case where the same retrovirus inserts in two different places- and the paper Willie's trying to argue over lists thousands- and Willie can't claim that all the identical viral insertion points are not evidence of common descent.

[#72], that's a good line. But see [#62]
[#71], see [#51].
[#70], see [#5] (dice example).
[#69] see above.

And for the PWND ERV fanboys present at the Jackson/Smith debate, see Evolanders PWND in creationism versus evolutionism debate.

Let's assume that ERV insertion really is random. then the logical inference is that ERVs shared by common descent must have come from an endogenization event in ONE individual. then all, for example, chimps and humans are descendents of that one individual ancestor. and this must hold true for all ERVs shared at the same genomic location in different species. I am no expert, but it seems like these shared ERVs are pretty numerous, meaning that all the species that share them also came from one individual. does this not strike anyone else as a bit hard to swallow?

@75: Actually, if you think it through, you'll see that all members of a species have a common ancestor if you go back far enough; read up on a little population genetics. For fun, get to grips with why the last common female ancestor of the whole current human race never met the last common male ancestor... Your problem is that you're thinking "came from one individual" in an Adam-and-Eve sense, when in fact the "last common ancestor" was a member of a population.

@74: my @73 kills your attempt at an argument and you know it. And one day you'll have to explain what the fuck an evolander is supposed to be.

@76: Isnt that a suv-species? ;-)
@75: Im not a scientist either, but I think you are on to the right line of reasoning here. Its just that final, hesitant straw-clutching sentence you need to get over and beyond.
If this simple, parsimonious explanation fits all available evidence, I personally find it a lot harder to swallow a goddiditinanonknowablewayevar model, which does not.

WW pretends to have answered my question (WW, what explanation do you have now for the common insertions at homologous sites in the genomes of chimps and humans?) in comment #71 with this: [#71], see [#51].

Unfortunately for WW, his comment #51 has no direct answer to the question other than a snide and irrelevant retort about restaurant owners and restaurant critics.

So I think that the record shows, per usual, that WW can provide nothing except snark and diversions in support of his notions. He can't answer questions, but constantly pretends to have done so in the hope that nobody notices his empty suit.

@dmso74

It's not hard to swallow at all...I really don't get why you don't understand that while these endogenization events, like mutations in general, occur in individuals and then take hold in the population due to drift, selection, or some other mechanism.

Really, I thought we went over this at the beginning of the thread.

For my sake, if not also for WW's, please clarify the evidence that germ cell ERV inserts are actually random (preferably proviruses not just LTRs).

Of the two papers Abbie cites as 'abused' by creationists (claim#2), one refers to HeLa cells (immortalised cervical cancer cells) and the exoviruses do show highly preferred insertion sites (as Abbie rightly points out) - HIV for example targetting active genes (presumably at unfolded DNA sites). This does not seem a solid place for data for obvious reasons. The other paper reports one and alludes to two other examples of independent same site insertion.

Can I also ask clarification for why the CERV 1 family is not found in both man and orangutans, but is in other 'closer' primates (I recognise only 4% of these insertions are thought to be orthologous)? (http://biology.plosjournals.org/perlserv/?request=get-document&doi=10.1…)

The same question applies to the CERV 2 family not found in man, orangutan, but it is found in orthologous sites in 'closer primates' and macaques (supposedly an older common ancestor, fig.5)(http://genomebiology.com/2006/7/6/R51). The authors also write, 'we were able to detect pre-integration sites at those regions in the human genome orthologous to the CERV 2 insertion sites in chimpanzees, effectively eliminating the possibility that the elements were once present in humans but subsequently excised.'

Finally isn't the site for the recent CERV30 insertion (so called HERVK 10) orthologous between chimps and humans (1p31)?

Doesn't this make arguments for common descent based on orthologous insertion sites less likely, unless the standard trees of descent are mistaken?

dmso74 (#75)

I'm not sure if what's giving you trouble is that you're assuming the first individual who developed the ERV is also the most recent common ancestor of the population in question. If so, you're mistaken. The ERV was most likely endogenized by an individual who lived some time before the MRCA and that ERV would have existed for a time in a proportion of the population but not every single individual in that population. Eventually, however, most likely just by chance, that ERV became fixed in the entire population and could be traced back to the MRCA.

Think of it this way: If there is a particular allele that you share with every single one of your cousins on your father's side then one of your paternal grandparents must have also had that allele. That grandparent is also the MRCA of you and your cousins. However, that grandparent was most likely not the first person to possess that gene.

This is just basic population genetics, BTW, and has little directly to do with evolution. Even if you're a creationist, you still have to accept this.

dmso74 (#75)

I'm not sure if what's giving you trouble is that you're assuming the first individual who developed the ERV is also the most recent common ancestor of the population in question. If so, you're mistaken. The ERV was most likely endogenized by an individual who lived some time before the MRCA and that ERV would have existed for a time in a proportion of the population but not every single individual in that population. Eventually, however, most likely just by chance, that ERV became fixed in the entire population and could be traced back to the MRCA.

Think of it this way: If there is a particular allele that you share with every single one of your cousins on your father's side then one of your paternal grandparents must have also had that allele. That grandparent is also the MRCA of you and your cousins. However, that grandparent was most likely not the first person to possess that gene.

This is just basic population genetics, BTW, and has little directly to do with evolution. Even a creationist has to accept this.

Sorry for the double post.

dmso74... I think I recommended in my first post that you check out what a most recent common ancestor is. It should explain everything.

Re [#78], okay, let me keep this simple for you. The price for questioning is not having an alternative explanation. If you were to question my assertions regarding quantization error not coming from an actual stochastic process, I would explain in more detail, giving references to scientific and engineering literature if necessary, and I wouldn't demand that you first provide an alternative explanation.

Only evolanders require questioners to have an alternative ready before addressing skeptical questions. The restaurant critic analogy is perfect, not irrelevant.

Regarding [#79]'s response to [#75], genes are transferred to descendants. Genetic osmosis among unrelated individuals is not a plausible "other mechanism" as far as I know.

Hence, dmso74 still has a good point that you did not address, viz., that under the assumption that ERV integration cites are random, *and* the additional and implicit assumption that independent insertions are never able occur at the same location, then instances of identical insertion points in two different creatures *must* mean that the two creatures descended from the same *individual*.

This second and implicit assumption may or may not have been an intended target of dmso74, but it is a key issue.

Specifically, under this implicit assumption, it is not even possible to differentiate two unrelated individuals sharing an ERV at the same location due to coincidence from the hypothesized common descent conclusion. The common descent conclusion is a logical consequence of the implicit assumption, which is why I am asking for scientific justification for the assumption.

[#82], your MRCA point is valid, but it in no way invalidates dmso74's point. If an ERV is present in a population, every individual that has the ERV at the specific integration point, under the assumptions made above, must have descended from the original synthesizer (OS) of the RV. If the ERV is universal, than every individual in the population is descended from the OS. Even if that OS is not the MRCA, it is a CA. The OS can be a MRCA, or just a CA. But unless ERVs are spread through osmosis and not reproductively, dmso74's skepticism, which seems to be against common descent in general, has not been addressed.

As a prophylactic against evolander debate tactics from getting out of control, and evolanders gloating over a typographical error: I meant site not cite.

@cprs (#80)

Abbie's already written a post on CERV 1 (also known as PtERV 1). It's a fascinating story, if not a bit creepy (Zombie viruses! Brrr!), but the simple answer is our ancestors seemed to be immune to this virus, while chimps weren't. Nothing to brag about, though; the tradeoff is that this has left us more susceptible to HIV.

http://endogenousretrovirus.blogspot.com/2007/06/frankenstein-viruses.h…

With CERV 2, there may be someone here who know mores about this than I do, but it seems this could be simply explained by the ERV not being fixed in humans. This kind of touches on dmso74's questions. Not every gene our common ancestor possessed is going to be fixed in a population (if so, we would be clones) and some of those genes could simply be lost entirely over time. It's worth noting that, in the paragraph just before the section you quoted, the authors mention that CERV 2 was transpositionally active in chimps between 1.3 and 6 MYA, i.e. after the likely date of divergence between the human and chimp lines.

WW

I hate to break the news to you, but in science you really should have an alternative explanation in mind when you repeatedly question an explanation put forward by somebody else.

As long as you understand that you are not behaving scientifically, I guess you can get away with your whines and diversions. But if you really want others to take you seriously and answer your questions, maybe you should pay attention to how science works. It's not just a habit of your mythical evolanders; mathematicians, astronomers and other heroes of yours are respected precisely because they not only had questions, they had answers.

WW: your MRCA point is valid, but it in no way invalidates dmso74's point. If an ERV is present in a population, every individual that has the ERV at the specific integration point, under the assumptions made above, must have descended from the original synthesizer (OS) of the RV. If the ERV is universal, than every individual in the population is descended from the OS. Even if that OS is not the MRCA, it is a CA. The OS can be a MRCA, or just a CA. But unless ERVs are spread through osmosis and not reproductively, dmso74's skepticism, which seems to be against common descent in general, has not been addressed.

You've got it partly right. True the OS is likely a CA. But what's so special about that? It comes back to what I said to dmso74: This is basic population genetics. Even if you believe the human race just emerged from God's rectum fully formed, the fact remains you only have to go back a few thousand years and the world is full of common ancestors. After a certain point ("after" in the reverse chronological sence of going backwards in time), if a person is an ancestor to anyone living today, then he/she is ancestor to everyone living today. It may be hard to get your head around that fact, but it's simple mathematics and, as I said, would hold even if creationism were true.

It's already been said, but a look at the Wikipedia article on Most Recent Common Ancestor will make this clearer.

Shrunk,

Thank you, the wikipedia article did help (much more than "learn some population genetics" snark). i might have to do the math myself to make sure i really get it, but the family tree analogy helps.

fyi i am an academic biologist (obviously lacking in pop gen training), and nowhere close to a creationist.

Albatrossity, if what you say is true, scientific journals would only publish letters critical of papers if the letters also posited alternative explanations. If scientist A wrote a letter merely pointing out how an assumption, made in a paper written by scientist B, taken to its logical conclusion would produce a paradox, for example, under your understanding of "science" said letter would not be published as it puts forth no alternative explanation.

Forgive me if I don't believe you. Indeed, it seems to me that journal editors would favor response letters that analyzed the paper in question, and did not try to sneak in alternative ideas via the letter route, as opposed to vetting those alternatives through the more formally peer reviewed paper path.

WW

P.S. This is a blog, not a journal.

fyi i am an academic biologist (obviously lacking in pop gen training), and nowhere close to a creationist.

I realize that. Unfortunately, I accidentally posted an earlier edit of my response that inadvertently implied that you might be one. My apologies.

BTW, folks really should pop over to the YouTube link WW graciously provided us. It's quite amusing watching him eat crow and claim victory at the same time.

http://www.youtube.com/watch?v=viszQiV-0Us

I wonder if anyone has done any statistics determining the "mean time to insult" for the creation vs evolution debate, namely the average amount of responses before the entire conversation is reduced to exchanging insults. I'm guessing it is a low number.

Then again it is probably not a creation/evolution thing, but an internet thing. So much easier to start insulting when your not face to face.

Anyway, to try to stay on topic, I have a question for Mr. Wallace. I'm not sure what standard of evidence you would accept for randomness, but lets just hypothesize that Abbie does show the insertion is random, or indeed, perhaps not random, but that the virus will target one of 3000 or so entry points. Given that ERVs fall into a nested hierarchy pattern, creating a phylogenetic (sp?) tree that cross corroborates with the same phylogenetic tree created by alternate molecular evidence (such as mutations in a pseduogene), would this be evidence for you of common descent? What other explanation would you suggest can acount for this data? And finally ,obviously you are not convinced concerning common descent, but could you hypothesize what evidence you would be convinced by, if common descent were true, what would YOU expect to find in the pattern of genetics across multiple species?

Thanks,
Pete

Thanks for comments Shrunk - will pursue.

I hope [#91] isn't ignored....

Shrunk, Dr. Jackson has acknowledged an error, first pointed out by a Monday morning quarterback, in assigning the Morganucodon to the permian layer when it is in fact found in the triassic layers (the layers immediately above the permian layer). It is one point, found by a Monday morning quarterback, readily acknowledged by Dr. Jackson in an email to me.

I don't hold it too much against Dr. J., since he fist said the Permian layer was from 250 million years ago in evolutionary scale, but that the Morganucodon was from 210 million year ago. Both are about correct. But you may hold it against him if you wish. I like the video, too bad it is sullied by Dr. Jackson's error in assigning the Morganucodon to the permian layers instead of the triassic.

I posted my question before I had read all the comments. Mr. Wallace, you seem to suggest in your sixth paragraph of post 85 that if the sites are random, common descent is a logical conclusion. Is this correct?

Shrunk's comments about population genetics are true, though I have a hard time wrapping my head around the idea as well. Dawkins explains it well in "The Ancestor's Tale", about how given enough time, if you are the ancestor of anyone you will be the ancestor of everyone. And yet, most likely ALL of your particular genetic material will have been weeded out. Indeed long term you might be the ancestor to everyone and yet contribute nothing to the genetic pool.

Pete,

I don't know if insertion points are random, or if there is a latent pattern, or if an ERV can be coincidentally integrated to the exact same spot in two different individuals.

Good evidence in the context Smith's post would be a paper analyzing insertion points and concluding that they are random.

That would be a start. It is something I requested back in [#5], but still have not had provided by any of the evolanders here.

Others may proceed as though they are random, and follow that path as though the assumption were true, and that is not in and of itself invalid. Such lines of inquiry are common in science.

But asserting that they are random as part of an argument supposedly proving common descent, without some sort of scientific justification, is not science. It is sophistry.

You start out with assumptions of random insertion points, and indeed, an implied assumption that that rules out the possibility of identical but coincidental integration points in different individuals, and then say, "see, they weren't coincidental."

Regarding your other point, I am not convinced of macro evolution. I would be convinced if a repeatable experiment were devised to create a new species. Say, for example, a scientist were to perform a founder/flush cycle on some creature, creating a new population, splitting it, allow the two populations to go through a number of generations in a new environment with new selective pressures, where the number of generations is either fixed, or specified as a range, and after the successive generations are allowed to breed, one or the other population develops a new tangible physical trait, say antlers, or an additional nose, or a blowhole, that clearly marks it as a new creature.

This sort of thing has been attempted, e.g., Dodd's 1989 fruit fly paper describing her observations, but the best they could do as far as I understand it was generate more fruit flies. Sure, population A could eat Starch based food, while population B could eat maltose based food, and ~80% of the females surveyed from population A preferred to mate with males from population A, while only ~20% of the females surveyed from population A would bother to mate with males from population B. But they were all still fruit flies capable of and even willing to breed with one another.

That would be a good experiment, though I would quibble on one point, if you started with a fish any new trait would in reality be a modification of something the fish already has, so antlers are probably out of the question until many many many different modified something else's have taken place. Alas, sadly the experiment would probably not produce clear morphological differences for tens of millions of years or so. And once football season starts I would lose interest so we only have four months or so.

But back to my point, you didn't quite answer the question. Assuming for a second that the sites are random, AND (I suppose) assuming there is a nested hierarchy pattern (since you seem to suggest there might not be), assuming these things to be true would this be evidence of common descent?

WW

If you ever actually read letters in scientific journals you would know that scientists who pen such letters usually DO offer alternative explanations for hypotheses or conclusions that they disagree with.

There are certainly letters expressing opinions about such things as conferences or nomenclature, but a letter written to disagree with a published primary paper almost always includes not only the factual disagreement, but also an alternative explanation for the observed facts.

You really need to get out more into the biological science literature. It would save you from this sort of embarrassment.

Pete, you asked several questions, and I answered most of them. I am not able to answer your last question as stated, could you elaborate?

Albatrossity, I do read biology papers from time to time, and would read more if the ones I wanted to read were free and readily accessible. As it is, I have to ask biology professors to send them to me.

I'll have to take your word that biology letters almost always have an alternative explanation for the observed facts. I have not noticed that pattern in the non-biology journals I've read.

One other point, Albatrossity, I fell for your "observed facts" goal post shift, and actually quoted it. The example I was using was questioning an assumption used to draw conclusions about observed data.

Short of a letter alleging a paper fudged data, observed facts are not usually challenged, are they, Albatrossity?

WW: This sort of thing has been attempted, e.g., Dodd's 1989 fruit fly paper describing her observations, but the best they could do as far as I understand it was generate more fruit flies. Sure, population A could eat Starch based food, while population B could eat maltose based food, and ~80% of the females surveyed from population A preferred to mate with males from population A, while only ~20% of the females surveyed from population A would bother to mate with males from population B. But they were all still fruit flies capable of and even willing to breed with one another.

Well, if you think about it, this is not that surprising. Consider we are 6 millions years removed from our MRCA with chimpanzees. If you assume a generation time of 25 years for humans, vs 2 weeks for fruit flies, that means for fruit flies to achieve the degree of divergence we have from chimps would require over 9000 years. So if you're correct that an 80% degree of speciation has already been achieved with fruit flies, I'd say that's already way ahead of schedule.

WW: I like the video, too bad it is sullied by Dr. Jackson's error in assigning the Morganucodon to the permian layers instead of the triassic.

I see you like the video so much, you've now made it "private."

Using your numbers, I get ~41,500 years.

Your definition of speciation is strange. If you think mating preferences (as opposed to actual cross fertility) defines a species, you have a point. One of the problems with the word species...biologists keep changing what it means. Which is why I referred to novel, tangible features.

Some bacteria divide every 15 minutes from what I understand. Using your 6E6 and 25 numbers again, I get 6.8 years for divergence as great as what you claim in chimps and humans.

P.S. Based on early screening results, the film has evolved. See http://www.youtube.com/watch?v=sF2Aa_SudC0 (Morganucodon: Evolutionism versus Creationism) if you want to learn about the great rat grandmother evolutionists claim you have.

WW

You were claiming that you did not have to provide an explanation for observed facts (homologous sites of ERV insertions in chimp and human genomes). Your distinction ("The example I was using was questioning an assumption used to draw conclusions about observed data") is therefore irrelevant. In a typical example, author A details some observations and makes a conclusion about the explanation. Author B sends a letter to the journal saying that the observations, which are assumed to be correctly reported, can be explained in some other way.

That's what I am asking you to do. You have the same observations as we do. The conclusion of those who did the work is that common descent is the best explanation. I've asked you several times for your explanation, but you don't have one. By default, then, the explanation (common descent) that was proposed by the original authors is still the best one at this time.

Case closed, at least until you manage to give us an alternative explanation for those observations.

Pete, you asked several questions, and I answered most of them. I am not able to answer your last question as stated, could you elaborate?

I'm not sure what is not clear about the question, though I can see it was worded a bit funny. I assume you know what a nested hierarchy is. Biologists assert that, for instance, they have identified many shared ERVs that aren't just shared among primates but fall into a nested hierarchy. In your post I thought you seemed to imply that no such pattern existed, we can talk about whether that is true later. I think it is unless the data I have seen is completely fabricated. But skipping that discussion, for the sake of argument I want you to assume that indeed the ERVs fall into a nested hierarchy. Likewise, I want you to assume that Abbie could demonstrate that ERVs will not only insert themselves in one location but will pick randomly from many possible locations, say up to 100. If these two things were shown to you (1: they are in a nested hierarchy and 2: there is some randomness in viral insertion), would this be evidence for common descent?

I am not a biologist, but the case is not closed in my estimation. From what I can gather, the conclusion you stand behind is based on assumptions not yet backed up by good scientific evidence.

But from what you've given me....

Possible explanations for homologous sites of ERV insertions in chimp and human genomes:

1. Under the assumptions: that ERV insertion sites are random or at least stochastic enough (note the biologist's mathematical ambiguity here); that homologous ERV integration sites cannot possibly be coincidental in two different species; that ERV markers really came from some long ago RV infection at just the precise instant necessary (just so); that extrapolated genetic clocks work, and have always worked, ah, like a clock, within a specified margin of error; and so on and so forth....common descent.
3. Latent functionality. Latent in either the sense of not currently known or not currently active.
3.a. For example, an occult (in the clinical sense) checksum, CRC, hash, programmer signature, or comment of some sort.
4. And one of my favorites: Coincidence.

But I could speculate all day. Speculation is pointless. Show me the data. I don't have data. For example, I don't have, as requested in [#5], a cite to a scientific paper that found, and not just assumed, good scientific evidence that ERV sites are random, such as demonstrating a cause/effect relationship between a known random source, such as thermal noise, to ERV insertion point outcomes, and also backed up by an analysis of ERV site selection to show that it is likely stochastic, e.g., using the NIST/Florida State University Diehard battery test suites to test for randomness), etc.

Possible explanations for homologous sites of ERV insertions in chimp and human genomes:

I much more interested in the nested hierarchy of ERV insertions that creates the same phylogenetic tree for primates already established by other molecular evidence, namely figure 4.4.1 on this link (I'm sure your familiar with the link)

http://www.talkorigins.org/faqs/comdesc/section4.html#retroviruses

You might need to cut and paste that, I don't know how to post links. Comparing shared ERVs between humans and chimps is one thing, but when an entire nested hierarchy is created going back as far as new world monkeys, then any other explanation besides common descent, which explains this figure exactly, would have to be rather creative. And yet, this data is widely known so there must be some explanation by creationists. Even if insertion sites weren't random, that wouldn't explain why the insertions we have fall into this nested hierarchy. There would be no reason why a specific new world monkey species might not share one with humans and no primate "in between" (the standard phylogenetic tree). If these were found, indeed if we never found any sort of nested hierarchy because these were abundant, of any molecular data much less ERVs, I would consider common descent to be falsified, and indeed never would have been persuaded of its truthfulness in the first place (until several years ago I was a creationist.)

Willy, willy, you yourself cited a couple of papers showing retroviruses inserting at any one of _thousands_ of places. In order for you to deny common descent you need to show that typically retroviruses only insert at _one_ place. So your position is already falsified. How much simpler could this be?

By the way @dmso74, "learn some population genetics" was not intended as snark, it was an honest piece of advice. Sorry if it came across snarky. The stuff Shrunk pointed you at is, well, some population genetics :)

Wallace likes to pretend that each scientific question operates in a bubble as well - it makes it easier for him to be in denial of the facts. I say so because he's doing it at the moment - despite the *facts* that there are recorded ERV insertions all over the genome in various species, smack dab in the middle of SINEs and other areas, he instead demands a comparison with noise (which, by the way, the data should match pretty well if he were to actually look at it). That is, despite the fact that ERVs will insert in many different areas with widely divergent functionality/essentially no nucleotide-specific functionality, he likes to pretend that there's still some latent pattern that can't be excluded, as if it would allow him to avoid the probability argument (it doesn't).

It's all very sad.

Also, why is it that the people having difficulty with this stuff say that the *only* way an identical insertion point of the same ERV is by common descent? That's not the argument at all: it's that the probability of a fairly random ERV insertion happening in that same place over and over and over again, just happening to form a nested hierarchy, is quite unlikely. Instead, common descent explains this pattern of *inheritance* very nicely and it already well-proven in its own right.

But I could speculate all day. Speculation is pointless. Show me the data. I don't have data. For example, I don't have, as requested in [#5], a cite to a scientific paper that found, and not just assumed, good scientific evidence that ERV sites are random

If you had bothered to read as far as Table 1 in the paper you cited in #32 (getting the first author's name wrong, too), you would have noticed that different experiments with the same viral vector produce different integration sites. The integration sites are in the NCBI database, so you are free to check the data if you don't believe them.

For example, an occult (in the clinical sense) checksum, CRC, hash, programmer signature, or comment of some sort.

Does that programmer sneak into cell cultures to comment on ongoing experiments?

WW

Thanks for finally addressing the question. It's interesting that you can talk endlessly about stuff, and yet finally admit you haven't read a single primary paper on the subject...

As for your explanations, here's my analysis.

1) Common descent - most likely, and, as others have mentioned, most consilient with lots of other observations.

2) you seem to have skipped this one.

3) Latent functionality - I'm going to proceed without your definition of that term, even though I know that is a dangerous move, since semantic games are your specialty. But there is no evidence for this at all. Can you provide an experiment to test this hypothesis?

4) Coincidence - incredibly unlikely from these data alone, and made even more incredibly unlikely by the consilience of the other data (e.g. chromosome 2 fusion, globin genes, GULO gene, etc.). As others have mentioned, the nested hierarchies in this case have been tested innumerable times, and have basically held up every time.

If you really wanted the data, you could find it. Do a google science search for "erv chimp human genome" and dig up the papers. Go to a decent library with a subscription to the Web of Science and do the same search. Get the free papers online (like this one) and get the rest via interlibrary loan. The folks who generated those papers have done a hell of a lot of work. You can do a little work yourself and get their papers to see if they really have overlooked all of your amateur disagreements with their conclusions. That really is how science works, at least in the real world.

Or you can remain true to form and sit on internet forums sniping at stuff that you don't really understand.

I don't have, as requested in [#5], a cite to a scientific paper that found, and not just assumed, good scientific evidence that ERV sites are random

you would have noticed that different experiments with the same viral vector produce different integration sites.

And you think that is good evidence? Pinewood derby racetracks with different inclines will produce different race times for a given set of pinewood derby cars, but that doesn't establish randomness, or even let you know how much randomness affects race times. Indeed, there is some randomness in a pinewood derby race time even if the incline is not changed, but other factors also explain differences in race times, such as lubrication wearing out, different orientations of the pinewood derby car from race to race, the moment of inertia, the center of gravity, which lane you're on, etc. You cannot attribute the entire distribution of race times in a pinewood derby race to randomness until you specifically target and attempt to characterize what effect randomness has on a race, and what effect other factors have on the race.

Meanwhile, Albatrossity shoots down the a restaurant critic for not being a world class cook, (as though you need to be a cook to be a good restaurant critic), I'd like to paraphrase an audience member from the debate:

Is there a single, published scientific paper that concludes, and not just assumes, that ERV integration points are stochastic?

Willy, willy, willy, you yourself have cited papers showing that these viruses randomly insert at any one of thousands (at least) of points. Didn't you _know_ that's what you were citing?

Oh, and willy: albatrossity is not telling the critic he needs to be cook. He's telling you that it would help if you could at least use your cutlery correctly and not try to eat your own shoes.

Another way of looking at the "restaurant critic" analogy failure - Of course the critic doesn't need to be a cook, but he would be in much better position to criticize if he actually spent some time eating at the restaurant! Merely reading a copy of the menu from the restaurant's website and talking to some other people who dislike the restaurant - most of whom also never ate there - means his supposed criticisms are baseless.

WW:

3127 insertion points and not a single repeat? Yes, I consider that good evidence for random insertion. Remember, this study was specifically looking for evidence of non-random insertion and reported some preference for particular types of sites (active vs inactive sites), but not to the point that specific sites are targeted. So, yes, that's a conclusion, not an assumption. If they had found those 3127 insertions were limited to, say, the same five or six specific sites, instead of 3127 completely different sites, then they would have concluded that insertion is not random and, furthermore, that ERV's can no longer be used as evidence for common descent. They didn't find that, so random insertion and ERV's as evidence for common descent is confirmed. Are you really so dense you can't understand this?

3127 insertion points and not a single repeat? Yes, I consider that good evidence for random insertion.

This would not be evidence for pure randomness. But it is evidence that the ERV does not insert itself into the same spot, or even one of merely 1000 spots. Though I'm sure if they tried an 3128 insertions, they would probably get 3128 spots, lets be conservative and assume that the most we know is that the ERV will insert itself into a spot with odds 1/3127. If chimps and humans share one, that is unlikely, but not terribly so. But what if chimps and humans share 5 such ERV insertions. Now we are at (1/3127)^5. And yet, humans and chimps share much more then just 5. But that is not the best evidence, as I tried to make clear in my last post. The best evidence is that when we consider other primates, including gorillas, orangutans, etc, not only do we find they share ERVs in homologous locations, but when they are shared, the fall into a nested hierachy. If we find an ERV we share with a new world monkey in a homologous position, the nested hierarchy pattern we find and indeed the prediction of common descent is that we will find it in every creature we share a more recent common ancestor with as well. That is what we find, exactly this nested hierarchy, once again as evidenced by figure 4.1.1 on
http://www.talkorigins.org/faqs/comdesc/section4.html#retroviruses

I would like to know from Mr. Williams an alternate explanation for this nested hierarchy.

Indeed, there is some randomness in a pinewood derby race time

Is there a single, published scientific paper that concludes, and not just assumes, that there is some randomness in pinewood derby race times, motherfucker?

You cannot attribute the entire distribution of race times in a pinewood derby race to randomness

Apparently you have forgotten what ERV said in the original post

Like Ive said a hundred times before, yes, some like to insert near active genes, and some like quiet genes, but exactly where a retrovirus inserts-- near which active genes, exactly which nucleotides are up/down stream, is random.

She did not attribute the entire distribution of race times to randomness. But thanks for flogging that strawman for us once again.

argh, "entire distribution of race times" should have been "entire distribution of insertion sites"

Is there a single, published scientific paper that concludes, and not just assumes, that there is some randomness in pinewood derby race times, motherfucker?

Aaaaand Windy wins this thread.

The foul mouthed Windy wrote:
Is there a single, published scientific paper that concludes, and not just assumes, that there is some randomness in pinewood derby race times, [deleted]?

Foul language aside--this is a great question. Let my answer serve as an example to Abbie, who still hasn't answered [#5].

It turns out that Dr. Scott Acton (Physics Ph.D./Texas Tech University--same school as the infamous Dr. Michael Dini) has studied the physics of the pinewood derby in painstaking detail. Furthermore, he has even put out a video summarizing his results, and it is also a useful example of the scientific method.

This video would be great for some ERV readers, because in it, he teaches about characterizing and isolating variables, coming up with and testing hypothesis, performing simulations, and, best of all, characterizing the magnitude of random effects.

He did it in a way that a 7 year old could understand (my 7 year old son understood it), so it might be a bit challenging for some ERV fans.

But take a gander at Physics and the Pinewood Derby.

(And no, my son did not win the Pinewood Derby, but that is because he built the car himself, and was not allowed to take full advantage of the conclusions presented in the video, as they were beyond his dexterity. He did pretty well, though, considering he's 7.)

...you yourself have cited papers showing that these viruses randomly insert at any one of thousands (at least) of points. Didn't you _know_ that's what you were citing?

You mean the paper that Abbie first wrote about, and in which the authors observed that there was a _bias_?

3127

Please, see [#5], where I preemptively addressed this issue.

3127 different sites don't matter. A completely deterministic process can result in 3127 different outcomes.

And while assuming that a random model as a basis of scientific reasoning and investigation can be justified in some situations, it is not good evidence that the random model is an accurate reflection of reality.

I've already given examples, from quantization error, to rolling a die to see if it is fair, to illustrate why a model that might be useful in one application is not necessarily a reflection of reality.

In order to provide good scientific evidence that a random model is an accurate representation of a physical process, you need to specifically investigate this, isolating all of the other variables that you are able to isolate.

Pete, I'll process your reasoning, give me some time. Meanwhile, do you know of a paper that concludes that ERV insertions are not deterministic, but stochastic, and doesn't just assume they are stochastic?

To anybody:

Once again, I'd like to paraphrase an audience member from the debate:

Is there a single, published scientific paper that concludes, and not just assumes, that ERV integration points are stochastic?

Mr. Wallace,

Thank you. Please do explain the nested hierarchy of ERV insertions. Who knows, you might actually convince me. I was open minded enough to be convinced that common descent was true, after 28 years of life and at least 14 years of being an active creationist, so it is clear my mind can be changed by evidence. But since this pattern is clearly explained by common descent, I'm going to need a very very good explanation for what other explanation could explain it (apart from the God made it that way to test my faith explanation).

Pete, I am going to do a mathematical analysis under various assumptions for you. I've started looking at your figure. Do you know how many ERVs are known to exist in human DNA? If you could provide a cite, all the better.

Nevermind, I'll just assume Abbie's figure of 98,000 is correct.

Pete, (or anybody else) is this a fair representation of the data we are talking about?

P.S. Mark Chu-Carroll, speak now or forever hold your peace.

Willie, since we've established that retroviruses _typically insert at any one of a large number of sites_, your entire argument already failed. We know _we can't predict where a given insertion will happen_ and _ it could happen at any one of many places_; your own cites establish this, so you don't get to argue against it. All you're left with is arguing about whether the universe is deterministic or not; which is unknowable and irrelevant.

I think a crucial point is being overlooked here (by one of us, that is.) No one is claiming that retroviral insertion is an entirely stochastic process. As Abbie wrote above, "...yes, some like to insert near active genes, and some like quiet genes, but exactly where a retrovirus inserts-- near which active genes, exactly which nucleotides are up/down stream, is random."

The only point of dispute is whether retroviruses have "preferences" for specific sites sufficient to result in every single primate having ERV's at those sites, without invoking common descent at the most likely explanation. As I've said before, at a bare minimum we need at least a single documented example of two independent yet identical retroviral insertions before we can begin to consider this hypothesis as even a remote possibility. To date, WW has yet to provide even a single such instance, so his hypothesis is a complete non-starter. Arguing that retroviral insertion is not completely stochastic is irrelevent, because we've already concluded that to be the case. What is lacking is evidence that the deterministic nature of retroviral insertion is sufficient to produce universal fixation of identical ERV's in unrelated species. (And, yes, this doesn't even yet address the issue of nested hierarchies that Pete has raised, and that WW is only now starting to "process" despite having expounded on this topic as nauseum for how long now?)

Another issue that has been ignored: Abbie has cited this paper in her "Creationist Claims about ERV's" post:

http://www.genetics.org/cgi/content/full/158/2/769

Now, most of this paper admittedly goes over my head. But from what I can understand, the authors were able to identify two separate retrotransposon insertions that occurred at the exact same site that occurred 12 million years ago. IOW, even if identical separate insertions had occurred, it is possible to detect this. To me, that clearly demonstrates that ERV's as evidence of common descent is not just an assumption, but an empirically verifiable conclusion.

1. It would be helpful to have a definition of nested hierarchy,
and I would hope for something more specific than this: http://evolution.berkeley.edu/evosite/lines/IVDhierarchies.shtml

If anyone's read Michael Denton's critiques of evolution you'll appreciate how this is precisely the ground from which he argues, in fact talkorigins arguments about cytochrome c (4.1, a few sections above their dated review of ERVs cited here several times) are the very substance of the argument he uses against both gradualism and common descent. I'm sure by using LTR comparison & other methods of dating, by showing the inverse correlation between insertional and sequence polymorphism, the nature of the nested hierarchy for ERVs can be shown to be more refined, but it would be nice to see a definition concisely in print. It would of course assume all ERVs are exogenous in origin, and involved in complex host function by fortuitous accident.

2. (minor point) WW, please correct old world monkey spelling in your data table.

3. CERV 1 or PtERV1 family.
Abbie's interesting Frankenstein post explores reasons for lack of human infection with CERV1 - but is hardly illuminating on the problem of a lack of human orthologues for CERV 1 (most of its insertions of course are not 'orthologous'). The problem is accentuated by the date for CERV1 being calculated at older than the divergence date for man and chimp. Perhaps the clock is not so reliable?

How does one explain the report from the paper I cited that at least 6 human apparently orthologous sites were deleted without trace?

More troubling, how does one explain that the same six orangutan sites were deleted without trace(assuming orangutans share a common ancestor with chimps, baboons and humans)?

The authors address this implication by claiming 2 of these sites were homologous insertions with the same insertion sites and not orthologous, because of BP differences between macaques and chimps. That does sharpen the question of how confidently one can distinguish the two phenomena - Abbie's primary issue for this thread.

The same problem applies also to the CERV2 family. This is not a single recombination/deletion but 2 site losses from different branches of the evolutionary tree for both humans and orangutans.

I don't doubt a good explanation can be conjectured, and I welcome reading them, but it does suggest the case for common descent from ERVs proves too much.

IIRC Denton attempts to critique evolution because he thinks that bacterial genes should be more similar to worm genes than they are to human genes. He is wrong, for obvious reasons.

cprs:

I'm not sure what you're failing to understand with the CERV 1 data. As the paper says itself:

Our data support a model where ancestral chimpanzee and gorilla species were infected independently and contemporaneously by an exogenous source of gammaretrovirus 3â4 million years ago.

That seems clear and simple. Humans and orangutans don't possess the ERV because we were never infected by the virus in the first place.

I've already offered an explanation of the CERV 2 findings above (which was based on an email correspondance with the paper's authors; you might want to try addressing your questions to them). It again touches on the issue of population genetics. If you research the meaning of "most recent common ancestor", you will find that not all of that ancestor's genes are passed on to all it's descendents. That is obvious; if they were passed on, we would all be identical clones. In the subsequent divergence of the human and chimp species from that ancestor, many genes were lost, and CERV 2 appears to have been among them. That's my, admittedly less than expert, understanding of the issue.

You're still displaying a fundamental misunderstanding of the ERV evidence. The emergence of a specific ERV in a genome is the result of a series of extremely unlikely events, so the existence of the same ERV at the same site in two different species is far far more likely the result of common descent than of those unlikely events occurring in the exact same way, down to the smallest detail, in the ancestors of those two species. Extend that to, not just two species, but several in a perfect nested hierarchy, and the odds become even longer. That there are differences in ERV's between species does nothing to refute this.

I have no idea what your section on nested hierarchies means, so I won't respond to it, other than to point you to this excellent video on the subject (He makes the script available in case he speaks too quickly for you to follow).

http://www.youtube.com/watch?v=5MXTBGcyNuc&feature=channel_page

Stephen Wells, which is the latest post [#128] applied to?

Shrunk [#129] wrote:

The only point of dispute is whether retroviruses have "preferences" for specific sites sufficient to result in every single primate having ERV's at those sites, without invoking common descent at the most likely explanation. As I've said before, at a bare minimum we need at least a single documented example of two independent yet identical retroviral insertions before we can begin to consider this hypothesis as even a remote possibility.

Apply different standards, much?

First, how could two independent yet identical RV insertions possibly be shown? If it met your criteria, based on the rather mathematically imprecise "stochastic enough" assumption, you would simply declare that they were not independent insertions.

Second, assuming even stronger evidence were found, say, an identical insertion found in orangutans and humans, but not chimps, evolution would be declared the winner here too with something like "Big deal. Natural selection creates that sort of stuff everyday."[1]

That is, if such a result were likely to ever see the light of day.

But let's assume that:

1. A researcher finds an ERV in humans and orangutans, but not gorillas and chimpanzees.
2. Let's assume she writes a paper titled "no so fast, evolutionary explanatory filter."
3. Let's assume it actually gets published in a "peer reviewed scientific journal" (because we all know how much biologists love seeing evidence against evolution).

How long before calls for the anonymous peer reviewer names to be released are made; how long before surreptitious campaigns orchestrated by the NCDE against the journal editor in charge are waged; how long before Abbie Smith and others in the PT-mafia start calling the researcher "creationist, Christian, anti-science, data fudging hobo"?

Third, why the different standards? On the one hand, you claim proof of common descent based on ERV and assumptions of random insertion points, but on the other, you know that you would not accept as falsification of this view data indicating a common ERV in humans and orangutans but not chimps.

This is how biology is done, but not science.

Footnotes
[1]Beware the believers (@ 0:28)

Mr. Wallace,

I can only guess what your graph is supposed to be reporting, perhaps you could give me a source (or did you create it from the figure I sent?)

For a good discussion of nested hierarchies, start with this link
http://www.freethoughtdebater.com/FEvolutionCase.htm
which itself is an intro to the separate and converging lines of evidence for common descent. Just a warning, since you guys are undoubtedly Christian, you will probably be offended by a few things this guy says. This is a clear introduction to the evidence of common descent, so I wish the author would remove the snarkyness.

Second, assuming even stronger evidence were found, say, an identical insertion found in orangutans and humans, but not chimps, evolution would be declared the winner here too with something like "Big deal. Natural selection creates that sort of stuff everyday."[1]

I would find this strong evidence against common descent. Has such an insertion been found? It would still need to be explained why the rest of them our found in a nested hierarchy. If ERVs do insert in identical locations, I would expect to find no pattern among species. We should see some shared by humans and orangutans but not chimps/gorillas, some shared by chimps, new world monkey, and dogs, but not foxes, old world monkeys, and orangutans, some shared between humans, mice, and turtles, but not any other reptile or mammal, etc. Ie, there shouldn't be a nested hierarchy at all.

I don't think your hypothetical researcher would have any problem if the data could be reproduced.

Pete, it was from your TO link. I thought it was rather self explanatory. Each of the Ei for i=1 to 14 were the 14 ERVs in the TO link.

Which brings up a question for Abbie: There are 11 common ERVs listed at TO. You mention 14. Is the TO link old news? Please understand that not all of us are ERV graduate students, and that this is an honest question.

Pete, please provide a single source for me to analyze. Even if it is a scientific paper (I can get access to them, it's just not convenient--but in this case, it would be preferred, because evolander sites have been known to mischaracterize scientific research.). If you must synthesize multiple papers to justify your viewpoint, so be it....send me cites for all of the scientific papers directly related and commenting on ERV and common descent.

evolander?

@pete#137:

As in EVOLANDER! COME OUT EVOLANDER! WE HAVE YOUR WOMAN!

WW is a modern day analog to Malachi in Children of the Corn...blindly following charismatic religious leaders against all evidence.

Hmmmm, I originally learned about ERV insertions from "Coming to Peace with Science" by Falk. Since then I have seen the information reprinted in various forms across the web, and I believe Abbie has a description of it here on her blog. But I think the TO link itself explains it pretty well, and provides references for all of its claims. Following their own link, the figure itself comes from the following paper.
Lebedev, Y. B., Belonovitch, O. S., Zybrova, N. V, Khil, P. P., Kurdyukov, S. G., Vinogradova, T. V., Hunsmann, G., and Sverdlov, E. D. (2000) "Differences in HERV-K LTR insertions in orthologous loci of humans and great apes." Gene 247: 265-277.

Props to you if you actually go out and find this paper. I'm much to lazy for that. I find it a fairly reasonable assumption that if this paper did not in fact report a nested hierarchy of ERV insertions and TO is simply lying about it, someone would have pointed that out. It is nearly 10 years old now.

Jon, I had the same exact impression. Coinages are tricky things. They can make one look like a buffoon if one doesn't take care.

Ahh, the true WW character comes out in #133. First off, he has repeatedly avoided the question in #113 -

Latent functionality - I'm going to proceed without your definition of that term, even though I know that is a dangerous move, since semantic games are your specialty. But there is no evidence for this at all. Can you provide an experiment to test this hypothesis?

Secondly, he sets up a fantasy situation, with damaging data that he fervently wishes could be found, and acts as if it was real. His fantasy is complete with evil conspiratorial scientists suppressing data, and all the other trappings of the paranoid mindset that characterize his entire online persona.

Finally, he beats his favorite dead horse, that biology is not really science. Iin his tiny world, only math (and maybe physics) can be designated as science.

Those latter two are not useful additions to the thread, WW. If Biology is Not Science, why are you wasting your valuable time here? Particularly after you admit that you have read none of the relevant papers? Is it because it is beneath you to read those scummy biology papers? Perhaps if you had read those papers, and understood them without the creationist blinders, you would be able to propose a useful hypothesis to test one of your coincidental notions.

WW:

Apply different standards, much?

First, how could two independent yet identical RV insertions possibly be shown? If it met your criteria, based on the rather mathematically imprecise "stochastic enough" assumption, you would simply declare that they were not independent insertions.

I'm sorry, I thought you just had a slightly less than adequate understanding of what we were discussing. I didn't realize you don't even have the slightest fucking clue.

Demonstrating identical RV insertions would be trivially easy. That study we keep talking about? The one with the 3127 RV insertions? Suppose those were not found at 3127 distinct sites, but at 3126. That would mean two of them were at identical sites. Are you following so far? Suppose they were only distributed among 6 different sites. That would be very strong evidence that retroviruses target specific sites, and would essentially kill the ERV argument for common descent (though if this were true, then I can't see how a nested heirarchical pattern could result).

Do you follow what I'm saying now? To support your argument, it is not enough to say that RV's tend to insert in certain general regions of the genome. We already know that they do. But to support your argument, you need to demonstrate that RV's will target, not certain parts of the genome, or even specific genes, but specific base pairs. In order to demonstrate this, you must find at least one example of an RV inserting into the same base pair in two individuals. Do you know of such a case?

If you have two separate ERV's at two distinct sites, those have resulted from separate insertions. It doesn't matter whether they are a single base pair apart, or located on entirely different chromosomes.

Do you get it now? If not, maybe you can ask your seven year old to explain it to you.

But let's assume that:

1. A researcher finds an ERV in humans and orangutans, but not gorillas and chimpanzees.
2. Let's assume she writes a paper titled "no so fast, evolutionary explanatory filter."
3. Let's assume it actually gets published in a "peer reviewed scientific journal" (because we all know how much biologists love seeing evidence against evolution).

How long before calls for the anonymous peer reviewer names to be released are made; how long before surreptitious campaigns orchestrated by the NCDE against the journal editor in charge are waged; how long before Abbie Smith and others in the PT-mafia start calling the researcher "creationist, Christian, anti-science, data fudging hobo"?

Are you even paying attention? We've been talking about almost exactly that just above (true, it's an ERV in common with chimps/gorillas and missing from humans/orangutans, but close enough). You'll note that none of your predicted responses have arisen from that paper. Although in this case, the differences resulted from infection after the process of speciation had begun, in general common descent does not predict that ERV's, like any other allele, will not be lost as the process of speciation continues. Remember genetic drift?

Not all of the differences between us and chimps need have resulted from mutations. Some are just different alleles from the common ancestor that have been retained in one line, but not the other. However, the identical genes indicate common descent. Think of it: Might there be some genes that your brother inherited from your grandfather that you did not? Does this mean that you and your brother don't share a common ancestor? However, if there was a new mutation that had developed in your grandfather that you and your brother shared, that would be sufficient to prove you and your brother having been descended from him regardless of whatever genetic differences there may be between the two of you.

First Pete and Stephen, isn't it wiser to be familiar with the arguments of your critics and not caricature them? Denton's case (and though he was early affiliated with DI he is no longer, and is not a creationist in any ordinary sense) is that genetic and protein sequences correlate closely with physiological and anatomical similarities, no big surprise - it emphatically doesn't show lineal descent - a typological critic of Darwin in his own day if he could access it would use the molecular biological data to make his case against 'the Origin'. Denton was driven to his sceptical conclusions by the data, despite the storm of anger and loss of reputation he knew he'd face. He used a nested hierarchy for cytochrome c sequence differences to ilustrate his case. That's why Pete your falsification implies a lack of appreciation of how your opponents think.

ERV nested hierarchies however are different and more interesting because they're considered exogenous in origin.

I'll read the pages you recommend (thanks for the gentle forewarning, Pete) - but dealing with blasphemy, mocking and inanities on sites promoting evolution is all too familiar - sadly it reveals much more than is intended.
Convergent evolution, alluded to so often at freethought, is masterly tautology - read a little of the tortuous history of psychoanalysis and you'll realise afresh the dangers of a overly plastic theory. Alone it's little more than black magic.

Shrunk, I have of course read the two groups of authors' interpretations of their findings CERV 1 and 2, but the data they cite indicates homologous ERV insertions which do not match the evolutionary tree, they would usually be called orthologues - but aren't here, they're attributed to cross infection. That's precisely the problem.

I follow the pop gen and genetic drift arguments, but why should both orangutans and humans lose all the apparent 'orthologues' of both large families, that does seem convenient reasoning.

As to the challenge about identical insertion sites for different ERVs - isn't Abbie's own example sufficient?

WW for reference the two main sources I've been using are both freely accessible, here they are again:

http://genomebiology.com/2006/7/6/R51
http://biology.plosjournals.org/perlserv/?request=get-document&doi=10.1…

Abbie's example of course is here:
http://www.genetics.org/cgi/content/full/158/2/769

At the risk of being a blabbermouth, there's one other point I'd like to make. When Pete says:

I would find this strong evidence against common descent. Has such an insertion been found?

I respectfully suggest this shows a misunderstanding of the nature of the ERV evidence. As has been mentioned, evidence of this type has been found, but is not evidence against common descent. ERV's cannot be used to falsify CD; they can only be used as evidence in its favour. The most creationists can do is demonstrate some mechanism besides CD that could explain identical ERV insertions arising in different species. However, that would still not disprove common descent.

What ERV's do accomplish is to completely, finally and utterly falsify the "hypothesis" (if it may be dignified with the term) that humans are the result of a separate act of creation, and not related to any other species. In other words, while ERV evidence is not necessary to prove common descent, it is sufficient. That's what Abbie means when she says, "if Darwin and Wallace decided to open a resort and spa in Cuba instead of going into science, if every fossil was still hidden-- The second we found ERVs, common descent would have smacked us in the head like a sack full of doorknobs."

As to the challenge about identical insertion sites for different ERVs - isn't Abbie's own example sufficient?

OK, so there we have it: One single example of an identical insertion (Which the investigators were incidentally able to distinguish as two separate insertion events)out of how many hundreds of thousands of ERV's going back at least 30 million years. So, can someone really good at math calculate whether this is sufficiently "non-random" to explain every single individual human, chimp, orangutan and gorilla having ERV's at exactly the same site? Or should we just go with my gut feeling that the answer is "Not a chance."

Braveheart,

you seem to have overlooked that science cannot prove, only disprove. That's what the principle of parsimony exists for.

Let me simply repeat comments 70 and 72. Either you provide evidence that retrovirus insertion is not random, or you give up and accept that repeated insertion in the same places in a single consistent tree-shaped pattern is astronomically financially unlikely, so unlikely it can be safely dismissed several billion times over.

Let's assume that ERV insertion really is random. then the logical inference is that ERVs shared by common descent must have come from an endogenization event in ONE individual. then all, for example, chimps and humans are descendents of that one individual ancestor. and this must hold true for all ERVs shared at the same genomic location in different species. I am no expert, but it seems like these shared ERVs are pretty numerous, meaning that all the species that share them also came from one individual. does this not strike anyone else as a bit hard to swallow?

No, why?

Ever heard of Mitochondrial Eve and Y-Chromosome Adam? That's how it works. Just more slowly in most cases â but time is always available.

Albatrossity, if what you say is true, scientific journals would only publish letters critical of papers if the letters also posited alternative explanations. If scientist A wrote a letter merely pointing out how an assumption, made in a paper written by scientist B, taken to its logical conclusion would produce a paradox, for example, under your understanding of "science" said letter would not be published as it puts forth no alternative explanation.

Forgive me if I don't believe you. Indeed, it seems to me that journal editors would favor response letters that analyzed the paper in question, and did not try to sneak in alternative ideas via the letter route, as opposed to vetting those alternatives through the more formally peer reviewed paper path.

WW

P.S. This is a blog, not a journal.

Erm...

1) It seems to me that you believe there's a difference between "paper" and "letter" in scientific journals. But there isn't (except that "Letters" have three pages in Nature, "Articles" have five, and "Brief Communications" have about one). All of these are papers, and all of these are therefore peer-reviewed. If I've correctly interpreted what you mean, you don't live in the same world as the rest of us.
2) There aren't different kinds of science in blogs vs journals. Science is science. I mean, what did you think!?! That you're allowed to get away with arguments from ignorance and personal incredulity because this here is a blog!?!

the permian layer

In just three words, you have revealed profound ignorance on geology and on stratigraphic nomenclature. Congratulations.

<headshake>

There isn't just one layer per period (really, how did you imagine sediment deposition? Did you ever imagine it at all!?!), and period names are capitalizedâ¦

Regarding your other point, I am not convinced of macro evolution. I would be convinced if a repeatable experiment were devised to create a new species.

Define "species".

I'm completely serious. There are at least 25 different definitions in the literature, and depending on the definition there are between 101 and 249 endemic bird species in Mexico. Please pick one.

This sort of thing has been attempted, e.g., Dodd's 1989 fruit fly paper describing her observations, but the best they could do as far as I understand it was generate more fruit flies.

<headdesk>

"Fruit fly" is a term like "mammal". Under any definition there are thousands of species of fruit flies.

<headdesk>

TSIB.

One of the problems with the word species...biologists keep changing what it means. Which is why I referred to novel, tangible features.

Define "novel", "tangible", and "feature". Sorry if that sounds like I'm nitpicking; I'm not.

[â¦] if you want to learn about the great rat grandmother evolutionists claim you have.

<headdesk>

Look. I could understand if you called it a shrew. Sure, it's as far away from shrews as it is from rats, humans, whales, and so on, but at least it hasn't got gnawing teeth and the jaw musculature and head shape that go along with this.

You mean the paper that Abbie first wrote about, and in which the authors observed that there was a _bias_?

A bias that doesn't come anywhere close to favoring single nucleotides over their neighbors.

When people say ERVs are inserted in the same place, they mean the same place, not a stretch of 10 or 100 nucleotides.

3127 different sites don't matter. A completely deterministic process can result in 3127 different outcomes.

Then suggest one. Or Ockham's Razor will get you.

P.S. Mark Chu-Carroll, speak now or forever hold your peace.

Huh? What makes you think he's reading this thread?

~:-|

Finally, he beats his favorite dead horse, that biology is not really science. Iin his tiny world, only math (and maybe physics) can be designated as science.

Which is funny, because math is not a science. It consists of definitions and tautologies; "1 + 1 = 2" is true because of the ways the symbols "1", "2", "+" and "=" are defined. It only uses internal contradictions to disprove ideas, not physical reality the way science does. Math is necessary for science, but it isn't a science itself; it's math.

If you have two separate ERV's at two distinct sites, those have resulted from separate insertions. It doesn't matter whether they are a single base pair apart, or located on entirely different chromosomes.

And if you have the same ERV at two distinct sites, those have resulted from separate insertions of the same retrovirus. Here, too, it doesn't matter whether they are a single base pair apart, or located on entirely different chromosomes.

BTW, I highly recommend this paper (pdf).

WW,

3127 different sites don't matter. A completely deterministic process can result in 3127 different outcomes.

It doesn't matter whether the process is completely deterministic. As long as it produces lots of insertions at lots of different sites, and almost never produces two insertions of identical ERVs at the same site, ERVs can be used to map common descent.

Similarly, an evolutionary program which creates "mutations" via a decent pseudorandom generator can have effectively identical performance to that of a program which reads in "genuinely" random numbers from a Geiger counter or something. "Deterministic" vs. "indeterministic" is a total red herring hee; -any natural process might be deterministic or indeterministic in principle. We can never tell for sure, and evolution doesn't care.

total red herring hee;

er, "here." What I get for fixing typos without hitting preview.

Denton's case (and though he was early affiliated with DI he is no longer, and is not a creationist in any ordinary sense) is that genetic and protein sequences correlate closely with physiological and anatomical similarities, no big surprise - it emphatically doesn't show lineal descent -

Denton now fully accepts common descent. I haven't read his latest book but since I agree with his concept of God created (via evolution) I doubt I would have much I disagreed with him.

I respectfully suggest this shows a misunderstanding of the nature of the ERV evidence. As has been mentioned, evidence of this type has been found, but is not evidence against common descent.

Okay, your right, let me rephrase. Its not evidence against common descent. But it would (does?) weaken the evidence the ERV markers do evidence common descent. Because they do so BECAUSE they are in a nested hierarchy pattern in this would be showing that they weren't. If we found them in common among many different animals clearly out of the phylogenetic tree will would build based on other evidence, then they would not be evidence for common descent. And actually, now that I have returned to proof read this paragraph, they might cause common descent doubt unless we could show they were not random insertions at all and the very point of much of this post is demonstrating they insert in many different locations. Since we know that is true, if we found the orthogoulous (sp) ones in a scattered pattern, we would lots of explaining to do.

But now you saying such a case exists, one that exists in both gorillas and chimps but not humans (not sure why orangutans are mentioned since that is an earlier branch so one can conclude the infection hadn't happened yet, unless an even more distant primate also has it?). For the chimp/gorilla but not human insertion I guess you are positing that after the insertion happened when we were homochimporillas, but it wasn't yet fixed in our population when the gorillas branched off, nor fixed in our population as homochimps when the chimps branch off, but later became fixed in the first two and was lost in us? Sorry, that was a mouthful.

Convergent evolution, alluded to so often at freethought, is masterly tautology

I don't think covergent evolution is overly plastic. If one started showing evolutionary convergence all the way down on the level of exact genetic base pairs, located in very distinct species but nothing in between, I would think that was too much coincidence for common descent to be true. But indeed, it is that the convergence is superficial that makes it not weaken the case of common descent but strengthen it. In the classic example of whale fins vs fish fins, we converge on a fin shape but only superficially, the whale is a modified walking mammal. We discovered it was a mammal for other reasons which then predicts those fins are modified mammal arms and hands and sure enough, pull back the skin and you find all the same mammal bones. If it wasn't superficial, indeed if bats, which are clearly mammals on all other traits, had bird wings, ie modified reptile arms, as opposed to modified mammal arms (or really long fingers in this case), that would be evidence of direct design to me and not common descent.

orthogoulous

Orthologous.

For the chimp/gorilla but not human insertion I guess you are positing that after the insertion happened when we were homochimporillas, but it wasn't yet fixed in our population when the gorillas branched off, nor fixed in our population as homochimps when the chimps branch off, but later became fixed in the first two and was lost in us?

That's entirely possible.

Another possibility is that the ERV was cut out in the human lineage; but in that case there should be a solo LTR (see purplish rectangle in the figures above), and I don't know if there is.

I'm afraid I may have caused more confusion than anything else with the discussion of CERV 1 and 2 (though in my defense, I'm not the one that brought them up).

Here's the paper in question:

http://genomebiology.com/2006/7/6/R51

As can be seen, it discusses CERV 1 and 2 which exist in chimps and some other primates, but not humans. However, there is no mention of the precise location of any of the insertions, presumably because these haven't been sequenced yet. Although, AFAIK, the distribution of these ERV's remains a bit of a puzzle, they don't affect the evidence for common descent at all, which is based on ERV's in identical locations. Sorry for any confusion.

Shrunk [#145] wrote: ERV's cannot be used to falsify CD; they can only be used as evidence in its favour.

It's good to see you admit this. And it is sadly not surprising. The evolution racket is an unfalsifiable ratchet. Evidence in support of evolution gets collected, prized, and trumpeted, and evidence against is ignored because it doesn't matter.

Pete, did you get that? Still convinced? They're whispering sweet nothings in your ear, and you're changing your stance as a result.

You could find 11 other ERV insertions that do not support the nested hierarchy you've been talking about, and it wouldn't matter I guess. I suspect that 111 ERV coincident insertions not supporting common descent with 11 supporting wouldn't matter either.

Not being able to falsify common descent means that tracking and reading ERV integration sites to support common descent is a metaphysical pursuit, and not a scientific pursuit (viz. a viz. CD, to reiterate the point.)

vis-a-vis, whatever.

"It's good to see you admit this. And it is sadly not surprising. The evolution racket is an unfalsifiable ratchet."

Saying that one particular phenomenon wouldn't falsify common descent is not the same thing as conceding that common descent is unfalsifiable. You'd be able to make this distinction, if you were not a retard.

Evolution is easily falsifiable. See here for a brief overview.

If you knew anything about evolution, instead of your strawman delusions, you would already know this.

Of course, I'm betting that you *do* know it, and you're just another Liar for Jesus.

Unrelated, cprs can kiss my atheist ass. Blasphemy is only blasphemous to believers. Reread ERV's tagline again. Only twits who have no actual arguments to make whine about "incivility" and "blasphemy". Real arguments get heated. You should listen in to actual scientists discussing actual science sometime.

Mr. Wallace,

I certainly think common descent is falsifiable. But regardless, I encourage you to continue to explore another explanation for the nested hierarchy of ERVs insertions, at least the ones from the diagram that has been linked several times. From my angle, even if the viral insertions always hit the same location (which they obviously don't, we know of at least 3127 from a study of 3127 attempts) that still wouldn't explain why they fall into a nested hierarchy. Common descent explains it exactly.

It turns out that Dr. Scott Acton (Physics Ph.D./Texas Tech University--same school as the infamous Dr. Michael Dini) has studied the physics of the pinewood derby in painstaking detail. Furthermore, he has even put out a video summarizing his results, and it is also a useful example of the scientific method.

I had a feeling that you were going to pull something like that with your pinewood derby example. But guess what, a video is not a published scientific paper! Man, even when you're setting a rhetorical trap, you get it wrong.

(Imagine the indignant whining if, in response to Willy-Wally's request for a peer-reviewed scientific paper, someone tried to offer him some amateurish video! Oh my!)

And from the webpage, looking at a section called "change and luck", it appears that they assume that a certain amount of the variation in race times is due to chance and luck!

3127 different sites don't matter. A completely deterministic process can result in 3127 different outcomes.
And while assuming that a random model as a basis of scientific reasoning and investigation can be justified in some situations, it is not good evidence that the random model is an accurate reflection of reality.
I've already given examples, from quantization error, to rolling a die to see if it is fair

Rolling a die, even a fair one, is physically a largely deterministic process. So your standards seem to be changing from one paragraph to the next.

Real arguments get heated. You should listen in to actual scientists discussing actual science sometime.

Real arguments might get heated, I don't think that makes it a good thing. Why would real scientists be uncivil to each other? Perhaps us humans are destined to always been angry and insulting but I think at least it would be an ideal that debaters focused on the issues and go light on the personal comments.

I do want to sincerely and without snark thank Shrunk, whomever he or she is, for the disclosure that ERVs can be considered as evidence for but not against common descent.

Enough said on this thread.

Willy bails, still not understanding anything, apparently astonished that things falling can be considered as evidence for but not against gravity.

I do want to sincerely and without snark thank Shrunk, whomever he or she is, for the disclosure that ERVs can be considered as evidence for but not against common descent.

Enough said on this thread.

And I knew, as I wrote that, that there was an excellent chance you would misconstrue it and quote mine it to support your argument. Still, if I pitched everything I wrote to your droolingly encephalitic level of comprehension, there would be no point in having any discussion here at all.

Did you not notice this part of my post as well?

What ERV's do accomplish is to completely, finally and utterly falsify the "hypothesis" (if it may be dignified with the term) that humans are the result of a separate act of creation, and not related to any other species. In other words, while ERV evidence is not necessary to prove common descent, it is sufficient.

An analogy: In investigating a robbery, the presence of the suspect's fingerprints at the crime scene is very strong evidence that he is guilty. The absence of fingerprints, however, does not mean he is innocent. Fingerprints can only confirm his guilt, they cannot falsify it.

If you disagree with me, provide a hypothetical example of an ERV pattern that would be impossible with common descent.

Echoing what Shrunk said, it is noteworthy that WW ignored the rest of that comment in order to quotemine the single sentence that resonated with his presuppositions.

Even more noteworthy would be an unpacking of this sentence: I do want to sincerely and without snark thank Shrunk, whomever he or she is, for the disclosure that ERVs can be considered as evidence for but not against common descent.

Given multiple opportunities, WW has failed to even whiff at designing a hypothesis to test his notions. So not only is there no evidence FOR special creation of humans, and plenty of evidence AGAINST it, there is not even a hypothesis which would allow us to test this notion. WW is a master at applying very strict standards to the conclusions of others, but consistently and spectacularly fails to apply those same standards to his notions.

Please come back when you have a hypothesis which will allow you to generate evidence FOR special creation, WW. Which will be, as we all know, never.

Carrying the analogy of the crime scene a bit further:

Let's suppose in this robbery there are multiple lines of evidence that point to a particular suspect as being guilty. There are several reliable eyewitnesses that confirm seeing the suspect break into the building. Surveillance cameras capture images of him entering thru a window, then leaving moments later with a heavily laden bag across his shoulder. The suspect has signed a detailed confession, including information that could only be known to the perpetrator of the crime. Samples of his DNA are recovered from the crime scene. After all this evidence has been gathered and the suspect charged and imprisoned, fingerprints are also found at the crime scene that perfectly match the accused's.

Knowing what a tight spot he is now in, the accused hires that crack criminal defence lawyer, William Wallace.

Come the trial, and Wallace is now cross examining the police detective. Ignoring all the other evidence, he goes directly to the fingerprints.

"Now, officer, you are pretty certain those fingerprints belong to my client. Just what makes you so sure?"

"Well, we recovered several prints from the scene that perfectly matched those from the accused."

"How do you know this was not a coincidence? How do you know the actual criminal was not someone whose fingerprints just happened to match my client's?"

"That would be impossible. Everyone's fingerprints are unique."

"Oh? And how do you know this? Do you believe that fingerprints are determined by completely random processes?"

"Well, not completely random, no. There are some patterns of whorls and such that tend to occur in many individuals. But this does not change the fact that every fingerprint is unique and can be distinguished from from anyone else's. No one has ever come across fingerprints from two different people that were identical."

"And you consider that sufficient reason to believe the prints from the crime scene are my client's? You believe this even though you have not examined the fingerprints of every single person alive to make certain that, in fact, no two prints are alike. Is that correct?"

"Yeah, pretty much."

"Well, thank you for your honesty. I guess the jury can decide whether they consider that sufficient reason. Now, these fingerprints seem pretty important to your case, don't they?"

"Well, there is all the other evidence. The eyewitnesses, the videotape, the DNA, the signed confession. Those are already pretty persuasive. But I guess the fingerprints are nice to have, too."

"So, tell me this, officer: If you did not have the fingerprints, would you still believe my client was guilty."

"Yeah, sure."

"Now, I'm going to ask you this one more time: Are you saying that, even if there were no fingerprints, you would still have sufficient evidence to convict my client?"

"Yeah, that's pretty much the case."

"AH HA!" Wallace exclaims, looking about the courtroom with a triumphant expression.

The jury and audience stare back, glassy eyed and incredulous, and the judge says, "Mr. Wallace, exactly how much are you getting paid for this?"

Why would real scientists be uncivil to each other?

Why would real scientists care about civility at all (one way or another)? Civility is not an argument. :-|

A bit more autism, please.

Why would real scientists care about civility at all (one way or another)? Civility is not an argument. :-|

But surely there is a difference between arguing about the evidence, and calling each other names.

Mr. Wallace,

Its your right if you don't wish to comment on this thread any longer. But I do think you need to take some time to "process" what it means for the ERV insertions to fall into a nested hierarchy. Given the insertions are an actual event in history, could not likely insert into the same place (probably not even 1 time, much less all the virus shared by so many species), but most importantly fall into a nested hierarchy pattern, I think the conclusion is inescapable. So inescapable that Answer in Genesis has to take the route of denying they are virus's at all. Indeed, it seems any person, group, or creationist organization that comes to understand the data as observed has had to take this stance, because if ERVs are viral insertions then they clearly evidence common descent. Whether it is possible they are not viral insertions, well I'm not a biologist. But it is clear they look so much like viruses that Answers in Genesis, instead of just assigning them some random genetic function, has admitted their relationship to viruses, but they conclude that the ERV are not insertions, but that Viruses themselves COME from the ERVs. I'll let you chew on the plausibility and theology of such a hypothesis.

Pete,

I'll be donig a post on ERVs soon enough. Maybe you can stop by and chat then. Since ERVs cannot be used to falsify common descent, it isn't a scientific test of the theory of common descent. Again, enough said, really.

Since ERVs cannot be used to falsify common descent, it isn't a scientific test of the theory of common descent.

I guess that's debatable. If something is able to produce irrefutable evidence for a concept, I would say it is a scientific test, even if it is not able to falsify the concept. However, what is beyond debate is that ERV's are able to falsify the notion that human beings are not related, by descent, to other organisms. Since the ideas of common descent and special creation are mutually exclusive, and there is no third option between the two, by falsifying one idea, ERV evidence it is able to confirm the other as correct.

If you're going to be quoting this thread in your article, be sure to include that. Otherwise, you would be deceptively quote- mining, and I'm sure you don't want to do that.

Mr. Wallace,

I disagree with you. But whatever. When you do make that post, please explain what ERVs are, and why they are in a nested hierarchy pattern. Any time I hear someone comment on them without mentioning the nested hierarchy, I take it as a complete non-answer and evidence they do not actually understand what the evidence is they are trying to refute.

Thanks,
Pete

Wow, how idiotic. No, Willy, DATA tends not to be falsifiable unless it was actually fraudulent or incompetently gathered. Falsifiability has to do with theories, hypotheses, etc. If we had ERVs in the genome and knew that they were inherited, by common descent we would expect them to form a nested hierarchy. If they didn't, we'd have to rethink the scenario, perhaps leading to falsification. The multitude of data in support of common descent wouldn't disappear if ERVs had conflicted with it, so it would all be weighed in kind.

Naturally, the data actually does support common descent and the prediction was thus (of course) supported. Falsification, as I listed above, was entirely possible, although not in the silly sense you seem to ascribe to it.

Might want to work on that poor middle school textbook understanding of the scientific method, WW. Then again, I don't remember even the most useless of texts confusing data for theory.

Maybe I should explain my thinking in saying that ERV's can only confirm, not falsify, common descent.

In trying to imagine the scenario that would be least consistent with CD, I came up with one essentially the same as what Pete described above (#135). That would be an arrangement whereby common ERV's are scattered in a chaotic, random matter among various species with no evidence of any pattern of inheritance or nested hierarchies. It would be as if each species just reached into a grab bag of random ERV insertions. Any two species could have a number in common just by luck, but it would not have any bearing on their phylogenetic relationship.

Now, suppose we actually observed this. Would it falsify common descent? I don't see how it would. All it would demonstrate was that common ERV insertions can occur in unrelated individuals without having been inherited from a common ancestor. It would certainly be a puzzling finding, and would falsify many of our accepted theories regarding the nature of ERV's. But it would not be evidence against common descent. It would just mean ERV's could not be used as evidence for common descent.

Does this make sense to everybody here?

As a side note, the kind of chaotic pattern of ERV insertions is what would be expected if WW's "theory" of non-random retroviral insertion were true. Since we don't observe it, this is strong evidence, if any more were needed, that his ideas are wrong.

Shrunk,

What if we observed ERV data and used it to construct a nested hierarchy which completely contradicted the current nested hierarchy we have now based on other evidences, such as comparative DNA. It would mean that our older lines of data which out current theories of common descent are based on would be contradicted by the ERV data, no?

Shrunk, I don't think falsification doesn't work like you think it does. When one comes upon data that conflicts with the prediction of a well-established theory, that is, one that has been quite predictive and is supported by a lot more data, you don't just immediately chuck it: you start thinking of explanations. That old data doesn't disappear, the entire idea isn't just thrown out.

Now, in the case of physics sometimes this *does* happen, largely because the realities they are dealing with, while often confusing, are much simpler. That simplicity allows them to have greater certainty with negative results. Other fields don't have this luxury, dealing with more complicated scenarios, so interpretation and weighing evidence becomes more difficult.

The basic point I'm making is that if ERVs were found to have a different but consistent nested hierarchy, it would cast doubt on common descent. It wouldn't immediately 'falsify' it without further study because one would still have to contend with the huge amounts of supportive data.

@174 is probably right; an ERV nested heirarchy which produced groupings like ( walrus , ( spider , artichoke ) ) and ( fruitfly , ( cholera , televangelists ) ) would be a bit of an issue.

Thus we snatch the straw from drowning Willie's grasping hands once more :)

Shrunk,

Since the ideas of common descent and special creation are mutually exclusive, and there is no third option between the two, by falsifying one idea, ERV evidence it is able to confirm the other as correct.

At least one of those premises is false, though. Special creation is mutually exclusive with common descent if sufficiently narrowly defined, but there are tons of other options. Multiple centres of divine creation, beloved by many biologists of Darwin's day; multiple lineages of organisms arising naturally on Earth via independent abiogenesis or panspermia events; and so forth.

Creationists like to claim that mainstream evolution and special creation are the only possible options, ergo any "weaknesses" of the first hypothesis are strong evidence for the second, but that's just their lack of imagination talking.

That would be an arrangement whereby common ERV's are scattered in a chaotic, random matter among various species with no evidence of any pattern of inheritance or nested hierarchies. It would be as if each species just reached into a grab bag of random ERV insertions. Any two species could have a number in common just by luck, but it would not have any bearing on their phylogenetic relationship.

Now, suppose we actually observed this. Would it falsify common descent? I don't see how it would. All it would demonstrate was that common ERV insertions can occur in unrelated individuals without having been inherited from a common ancestor.

I think the implications would be more serious than that. If each one of these ERVs was found across a whole species, or across a large chunk of a species, then it would appear to have been inherited from a common ancestor. And by measuring modern insertion rates or constructing molecular clocks, we could conclude that germ-line ERV insertions are quite rare (on a human time-scale); again, this would suggest that most observed ERVs have been inherited from the carrier's distant ancestors.

So we would have ERV-based patterns of common ancestry at the population and species levels, but not above that--just as if each species were independently created. This would be strong evidence against common descent, unless we could develop a good explanation of why ERV-based phylogenetics would suddenly fail above the species level.

OK, guys. You've convinced me. I hadn't thought of the possibility of a series of nested hierarchies that suggested multiple, independent lines of descent (What the creationists would call "microevolution within kinds"). While such a finding would be very difficult to reconcile with all the other evidence for universal common descent, taken on its own it would be better explained by creationism than by evolutionary theory.

So, to WW: This is probably of little relevence, since if you actually plan to write an article on this, you would obviously base it on more than an anonymous blog comment by someone with no known qualifications in the field. But just for the record, I no longer maintain that ERV evidence cannot falsify common descent.

Shrunk,
I was the 'culprit' who raised the CERV 1 and 2 families. The 2006 Genome study is based on a chimp whole genome search, as even the abstract explains, it identifies orthologues which requires determining their respective chomosomal positions, unless I have missed something major. So why claim otherwise? I am completely mystified by your statement.
'Of the 42 families of chimpanzee endogenous retroviruses identified in this study, 40 were found to have orthologues in the human genome, including 9 that were identified in this study for the first time [14] (see Additional data file 1). Two previously identified chimpanzee endogenous retrovirus families do not have human orthologues (Table 2).'

There is a serious problem here for common descent, though by no means insuperable.

As to Pete and other comments on convergent evolution, I don't think you have begin to grapple with the depths of the problem with the cursory nod towards fins, here's a short catalogue, http://www.thegreatstory.org/convergence.pdf. The collector is Darwinist, as her seamless but revealing extrapolation to human thought illustrates. Just ask the question, if these parallels had arisen in closely related branches, wouldn't they vindicate a (non existent) common descent? Look again at the highly similar tertiary structure for haemoglobin and myoglobin, ancient paralogs they are often called, but have you considered how their primary sequence shares only 6 or so amino acids out of about 140? There are many other examples.

As to poor old Denton, I am not surprised he has retracted his originally trenchant and wide ranging critique under the furious storm of personal attacks. No mild agnostic likes to be attacked as a campaigning creationist, when he isn't. Here's a short section from Nature's Destiny to show his current view, "The design of living systems, from an organismic level right down to the level of an individual protein, is so integrated that most attempts to engineer even a relatively minor functional change are bound to necessitate a host of subtle compensatory changes. It is hard to envisage a reality less amenable to Darwinian change via a succession of independent undirected mutations altering one component of the organism at a time." He's become a kind of mystical Lamarckian.

As to the danger of personal invective in science - I am surprised anyone who knows how such tactics hindered Lister, Harvey, Koch or a host of other pioneers has the courage to advocate such obscurantist tactics here. Ad hominems usually reveal more about their authors than their targets.
I also acknowledge, though, with all due respect to our mathematical colleagues, it's perhaps not the only obscurantist tactic used on this thread.

This is probably of little relevence, since if you actually plan to write an article on this, you would obviously base it on more than an anonymous blog comment by someone with no known qualifications in the field. But just for the record, I no longer maintain that ERV evidence cannot falsify common descent.

Interesting, thanks. So now we have something important to talk about, and I have more work to do.

Before I begin, at the talkorigins (TO) link in [#109], why were the rightmost three ERVs included in Figure 4.4.1? At first blush, it appears to be a form of deceptive presentation of data, but perhaps I am missing something. I mean, humans have more than 14 ERVs, and more than 3 ERVs not shared by the chimps et. al, right?

On a related note, Common ERVs is in my view an objective and better presentation of data than what is in the TO link at [#109]. It is presenting essentially the same data, leaving the implications of the hierarchy as an exercise for the reader. It even preserves ERV 12 through 14 (E12 through E14, though I don't know what makes 12, 13, and 14 any more important than E15 through E90000.

The TO presentation could be further improved with horizontal error bars representing best estimate of the time the RV is thought to have become endogenous, +/- uncertainty, and best estimate of time species were thought to have split, +/- uncertainty in time and species definition, all indicated.

Anyway, how would I go about finding as much information as I can about all known ERVs in the six species of animals and one species of humans trumpeted at Talk Origins, including the ERVs not listed in [#109]'s Figure 4.4.1?

I'd like to perform a mathematical analysis of data if such sequences exist in some database.

I'd also like a knowledgeable evolutionist to help perform an analysis and also construct some simulations. The simulations will of course be based on assumptions, and I want to come up with a reasonable set of assumptions, and also disclose them, and perhaps allow them to be tweaked so that various simulations can be performed.

Assuming this hasn't been done before (and it may have, which could save a lot of time), I think it would be a useful exercise to think about various possibilities.

Next, assume that, for the sake of argument, the species indicated in the "Common ERVs" (my representation) row headings are randomly permuted, and the ERV indices are now numbered 15 through 28.

Suppose a third chart is constructed by again randomly permuting the row headings, and numbering the indices 29 through 42.

And now, we will have, hypothetically, three different nested hierarchies (NHs) that could be constructed, one of which will support CD, and the other two, equally compelling, which would not, assuming the permutations resulted in a sufficiently different row order from the CD supporting E1 through E11.

Certainly, it seems to me, this sort of data would cause people like Abbie to rethink, at the very least, the theories about how ERVs end up at their current locations. But would it give any evolutionist pause to rethink CD?

Now, this hypothetical example could be taken further, with a variety of outcomes. For example, suppose that the strongest single NH supports CD, and the current tree of life, but two other only slightly weaker NHs of 10 common ERVs per nested hierarchy support two, drastically different from the first NH, of 10 common ERVS each, say E20 through E29 supporting NH2 and E30 through E39 supporting NH3.

Extending this example further, at what point does the nested hierarchy trumpeted by TalkOrigins [#109] become the equivalent of finding a shape in a cumulus nimbus cloud that strongly resembles Frosty the Snowman?

Shrunk, are you a biologist? A professor? An ERV researcher? Perhaps you could help me shine some critical light on the ERV evidence of CD.

For crying out loud, William Wallace thinks the universe is 6,000 years old. ERVs are the least of his concerns.

Dear William,
being none of the above, I offer a small start. There are at least 42 common ERV families in primates (CERV 1 and 2 are both lacking in man in orangutans), details in Genome reference Shrunk links again, Table 2.

CERV 2 for example in your table would be -(humans) +(chimps) +(bonobos)+ (gorillas) - (orangutan) +(macaques) - new world monkeys. The text cites 6 apparently orthologous sites, but many are not shared by all species, (Table 5)

CERV 1 would be 0(humans), 5(96)(chimps), ?(bonobos), 3(81) (gorillas), 8(81) baboons, 0(orangutan), 8(46)(macaques).
The numbers are apparently orthologous (total including non-orthologous sites), but there are qualification about the precision of the determination and the paper doesn't specify between which species the sites are deemed orthologous.
Taken from, http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1054887&rende…

I was the 'culprit' who raised the CERV 1 and 2 families. The 2006 Genome study is based on a chimp whole genome search, as even the abstract explains, it identifies orthologues which requires determining their respective chomosomal positions, unless I have missed something major. So why claim otherwise? I am completely mystified by your statement.

I think you are missing something. The 2006 study does not identify orthologous insertion sites between chimps and other apes that are lacking in humans.

As you noted above, the PLoS study they cite was able to unambiguously identify "95.8% of the insertions occur at non-orthologous regions". But what about the other 4.2%?

Within the limits of this BAC-based end-sequencing mapping approach, 24 sites mapped to similar regions of the human reference genome (approximately 160 kb) and could not be definitively resolved as orthologous or non-orthologous

So they were not identified as having identical insertion sites, they were identified as inserting within the same 160,000 base pair region! That's still quite a lot. Some of these "overlap" loci were shown to be non-orthologous at a closer look, and some couldn't be pinpointed to an exact location because of the repetitive sequence.

These two articles you cited are a little unclear at points, so I don't blame you for being a little confused. When they say things like 'the age of this virus family is inconsistent with the age of the human chimp split', they are just using it as a build up so that a couple of sentences later they can jump out of the bushes and go 'A-HA! This is how we resolve the inconsistency!' My old professor would have told them that a scientific article does not need to be a detective story...

'Of the 42 families of chimpanzee endogenous retroviruses identified in this study, 40 were found to have orthologues in the human genome, including 9 that were identified in this study for the first time [14] (see Additional data file 1). Two previously identified chimpanzee endogenous retrovirus families do not have human orthologues (Table 2).'
There is a serious problem here for common descent, though by no means insuperable.

It simply means that the retrovirus infections that created these two families occurred after the human-chimp split. These CERV families occur in other primates, but not at identical insertion sites to the chimps.

The 2006 article also says that "two CERV 30 (HERV K10) insertion polymorphisms have been identified in human populations". So, some humans have insertions that others lack. That is not a problem for common descent of humans, it simply means that some insertions are more recent than others.

Thanks Windy, most CERV1 insertions aren't orthologous and there's doubt about those that are - agreed. However there are at least apparent 12 hot spots for a number of common insertion sites between nonhuman primates, that alone is noteworthy, and the exact insertion site would be interesting to know.

Again there are apparently orthologous non human primate sites for CERV2 - there's a bit of brinkmanship as you suggest - and one is definitely whittled away, but there are up to six sites mentioned. None is specified except the representative one, and that by chromosomal locus not by sequence. I agree the non orthologous sites for these two families and CERV30 are irrelevant to descent, but just as they cite the CERV30/HERVK10 orthologue as indicative of human chimp ancestry, so the blemishless deletion of up to six orthologous sites of CERV2 is remarkable for the same reason.

Who's going to write to the authors?

Of course, I'm not suggesting they already have the answer to hand (maybe they do after 3 years) - merely to encourage its pursuit. Sorry re double post - was interrupted.

cprs,

However there are at least apparent 12 hot spots for a number of common insertion sites between nonhuman primates, that alone is noteworthy, and the exact insertion site would be interesting to know.

But those intervals donât seem to be common insertion sitesâthey were in the âambiguousâcategory to start with, and the authors were able to shoot down four of them as non-orthologous. The rest remained ambiguous, but the authors provide additional lines of evidence as to why theyâre probably not orthologous either.

I agree the non orthologous sites for these two families and CERV30 are irrelevant to descent, but just as they cite the CERV30/HERVK10 orthologue as indicative of human chimp ancestry, so the blemishless deletion of up to six orthologous sites of CERV2 is remarkable for the same reason.

No one is suggesting that they were deleted, thoughâin fact, the authors specifically say they werenât. Shrunkâs suggestion, which s/he says is based on correspondence with the authors, is that they simply never went to fixation in the human-chimp common ancestor in the first place. Then there would be nothing to delete--humans would be descended from members of that ancestral population which never had those ERVs.

Who's going to write to the authors?

How about you? It sounds like they're happy to talk about this stuff.

But those intervals donât seem to be common insertion sitesâthey were in the âambiguousâcategory to start with, and the authors were able to shoot down four of them as non-orthologous. The rest remained ambiguous, but the authors provide additional lines of evidence as to why theyâre probably not orthologous either.

Right! That's what I was trying to explain in #183, but this is a shorter and clearer way of saying it.

No one is suggesting that they were deleted, thoughâin fact, the authors specifically say they werenât. Shrunkâs suggestion, which s/he says is based on correspondence with the authors, is that they simply never went to fixation in the human-chimp common ancestor in the first place. Then there would be nothing to delete--humans would be descended from members of that ancestral population which never had those ERVs.

No, this is not consistent with the article at all (and I don't see where shrunk says anything about corresponding with the authors?). If there were ancestral polymorphisms at several integration sites of these ERVs, why would all of them have been lost by genetic drift in humans, but not in chimps? And particularly CERV 2 is way too old to have been maintained as an ancestral polymorphism up to the chimp-human split.

I think the authors are trying to get across the idea that these ERV families are likely the result of multiple exogenous infections in chimps, by emphasizing how unlikely the alternative is.

PS. It's worth looking at Figure 1 in the 2006 paper. Look at what sequences cluster closest to the CERV 1 and 2 families - there's a baboon virus, a feline virus, and our old friend the PERV! It doesn't seem unlikely that these virus families could have come to chimps via horizontal transmission.

A couple comments:

First of all, I did mention corresponding with the authors of the paper. I've been able to find the reply I received, which was rather brief, but to the point:

"Our findings are not incompatible with evolution. Transposable elements can be lost from (or added to) lineages over evolutionary time."

I have emailed the author again to inform him of this thread. I'll let you know if I receive a reply.

Second, the main point that seems to be overlooked here is that only ERV's found at identical locations (i.e. to the exact base pair, not just chromosomal regions or "hot spots") are relevent as data regarding CD. ERV's located at different locations are from separate insertion or transpositional events, and are not of any phylogenetic relevence. In this paper, I see no explicit mention of identical insertion sites for any of the ERV's.

Thirdly, since it seems to be a matter of some discussion, I'm a male. :)

Thanks Shrunk, I somehow missed the bit about the correspondence. But I think the authors are not referring to ancestral polymorphisms, but indels and new insertions after the human-chimp(s) split, to explain the differences.

Fair enough, but where precise sequencing does not confirm the insertion site, there are two important corollaries, strictly the use of the term 'orthologues' is presumptive only, and without further study none of the data from the 42 families of CERVs in this particular paper yet confirm monophyletic descent for any of the primates involved - the argument cuts two ways.

windy,

If there were ancestral polymorphisms at several integration sites of these ERVs, why would all of them have been lost by genetic drift in humans, but not in chimps?

I imagine the polymorphisms could have assorted geographically. The ERVs we're talking about belong to just two families, after all, and each family's the result of one or more exogenous infections by a particular virus or family of viruses. If that virus is only common in part of a species' range (because its vectors or carriers live there, or because that's where the species' Patient Zero happened to be, or whatever,) then couldn't the ERV family be initially confined to that area?

If our common ancestor had a geographical distribution of ERV families, and speciated allopatrically, then descendant species might end up inheriting different families.

But as you say, this obviously couldn't be the case for an ERV family if it really had arisen over ten million years beforehand!

And particularly CERV 2 is way too old to have been maintained as an ancestral polymorphism up to the chimp-human split.

Only if the age estimate the authors compute via sequence divergence is correct, and they themselves apparently doubt that, writing that the estimate is "inconsistent" with other facts they provide. In the two other cases of anomalously old ERV families--CERV 1 and CERV 3--they explain why sequence divergence might skew the age estimate high, and I think the same considerations are supposed to apply to CERV 2. (Their discussion of CERV 2 is, explicitly, largely a repeat of the bit on CERV 1.)

But I think the authors are not referring to ancestral polymorphisms, but indels and new insertions after the human-chimp(s) split, to explain the differences.

They rule out deletions entirely, though, writing, "Again, we were able to detect pre-integration sites at those regions in the human genome orthologous to the CERV 2 insertion sites in chimpanzees, effectively eliminating the possibility that the elements were once present in humans but subsequently excised."

I think the authors' main explanation is that their age estimates are simply wrong here. Either these families are the result of insertions entirely after the human/chimp split, as you suggest, or they're (slightly) older than the split and weren't yet fixed when it occurred.

cprss,

Fair enough, but where precise sequencing does not confirm the insertion site, there are two important corollaries, strictly the use of the term 'orthologues' is presumptive only,

But this paper (the PLoS one) does not claim that any of the insertion sites it covers are orthologous. It claims that 24 out of 299 are ambiguous, and that the other 275 are not orthologous. The latter claim doesn't presume anything; you don't need to precisely localize two insertion sites to confirm that they're not in the same place.

and without further study none of the data from the 42 families of CERVs in this particular paper yet confirm monophyletic descent for any of the primates involved - the argument cuts two ways.

Is there a reason it should confirm any such thing? This (the paper mentioning 42 families of chimp ERVs) was, well, a paper surveying chimp ERVs; it wasn't trying to establish anything about primate phylogeny.

Anton:

They rule out deletions entirely, though, writing, "Again, we were able to detect pre-integration sites at those regions in the human genome orthologous to the CERV 2 insertion sites in chimpanzees, effectively eliminating the possibility that the elements were once present in humans but subsequently excised."

For CERV 2, but the paper identifies several instances (Table 3,4 & Figure 6) in other families where the retrovirus was excised (leaving LTRs) or the whole region was deleted (no intact pre-integration site to explain).

cprs:

Fair enough, but where precise sequencing does not confirm the insertion site, there are two important corollaries, strictly the use of the term 'orthologues' is presumptive only, and without further study none of the data from the 42 families of CERVs in this particular paper yet confirm monophyletic descent for any of the primates involved

Err whut? They say they DID identify orthologues in all but two of the families. Just to see that they weren't kidding about the orthologues, I picked one of the ERVs from Table 2:

CERV 5 (HERV15) 20:22151622..22161290

The coordinates refer to the Ensembl genome browser, so this should be the view of the position of the ERV in the chimp genome.

I downloaded the sequence of "Contig71.30", which is a sequence assembly of the region, about 60,000 bp, which encompasses the ERV's ~9,700 bp. When I do a BLAST search of this contig against the human genome, it's a 99% match, so it would appear that the ERV is in the same place there (otherwise it would show a gap!)

It's not actually clear to me that when they use the term "orthologous" this necessarily means that the ERV's are located at the same site in the genomes of both species. It seems to me they are simply using it to refer to ERV's that have resulted from the same virus. Otherwise, that would mean that there are at least 40 identical ERV insertions between humans and chimps, which is much higher than any figure I have heard elsewhere.

windy,

For CERV 2, but the paper identifies several instances (Table 3,4 & Figure 6) in other families where the retrovirus was excised (leaving LTRs) or the whole region was deleted (no intact pre-integration site to explain).

That's quite true. It's only certain subfamilies in CERVs 1 and 2, and that single CERV 3 element, for which the inconsistency arose (no human orthologues, no apparent deletion, and clocked by their age estimator as older than the chimp-human split.)

Shrunk,

Otherwise, that would mean that there are at least 40 identical ERV insertions between humans and chimps, which is much higher than any figure I have heard elsewhere.

That's not too surprising, though. The vast bulk of chimp ERVs were unknown before this study, so no previous paper would have found anywhere near as many common insertion sites. Even nine of the human ERV families found to be orthologous were first identified in this study. (See the associated letter at http://jvi.asm.org/cgi/content/full/80/9/4640?view=long&pmid=16611924#T1 .)

Otherwise, that would mean that there are at least 40 identical ERV insertions between humans and chimps, which is much higher than any figure I have heard elsewhere.

If there are tens of thousands of ERVs in the human genome, it's hardly likely that most of them would have been inserted after the chimp-human split! If we in fact had less than 40 shared insertions, I'd say that would falsify chimps and humans as sister species...*

*just to be clear for Willy's and cprs's sake, this is a counterfactual scenario, we share more insertions than that. The paper identifies three types of ERV families: families where no new insertions have occurred after the chimp-human split, families which have orthologues *and* some new insertions in either of the species (indicating that the ERV has been active both before and after speciation), and families which occur only in chimpanzees. As we would expect if the species have recent common ancestry, the non-shared families are a minority.

If there are tens of thousands of ERVs in the human genome, it's hardly likely that most of them would have been inserted after the chimp-human split!

Is that true, though (Honest question, not rhetorical)? Of course, we would expect more ERV's to have been inserted into our genome prior to the divergence with chimpanzees. But since these are nonfunctional genes, and therefore not conserved by selective pressure, how many of these would survive to the present day? It could be argued that more recent ERV's (i.e. those inserted after divergence from chimps) would predominate in our genome, having had less time to be degraded by mutations. Otherwise, we could also expect to find the genome to be abounding in ERV's shared with all other organisms with whom we share a common ancestor, which of course is all organisms, period (limited by the fact, of course, that not all organisms develop ERV's). If that were the case, I would expect ERV's to make up an even greater percentage of our genome.

But I could be wrong, and welcome more informed opinions.

Is that true, though (Honest question, not rhetorical)? Of course, we would expect more ERV's to have been inserted into our genome prior to the divergence with chimpanzees. But since these are nonfunctional genes, and therefore not conserved by selective pressure, how many of these would survive to the present day?

Of course they are degraded over time, but that doesn't mean that they are lost that fast. From Wikipedia on ERVs:

There are many thousands of endogenous retroviruses within human DNA (HERVs comprise nearly 8% of the human genome, with 98,000 elements and fragments[7]). All appear to be defective, containing nonsense mutations or major deletions, and cannot produce infectious virus particles. This is because most are just long-lasting traces of the original virus, having first integrated many millions of years ago. However, there is one family of viruses that have been active since the divergence of humans and chimpanzees.

Otherwise, we could also expect to find the genome to be abounding in ERV's shared with all other organisms with whom we share a common ancestor, which of course is all organisms, period

You are making a false dichotomy here. You assume that either almost all ERVs older than the human-chimp ancestor should have been completely lost, or that you should be able to find ERVs from ALL of our ancestors no matter how old. Of course, the truth is somewhere in between. There are a lot of other non-coding loci that are shared between humans and some or all other primates, like pseudogenes and microsatellites, but none that are shared with all organisms.

Thanks to all, but esp to Windy, most interesting to see the raw data and how easily obtained it is with a good guide - indisputably highly homologous regions without gaps - and I can understand well founded the claim of orthologous sites is for CERV5 for example.

Given criteria as rigorous, the orthologous CERV 1 and 2 sites for man and orangutan are all indisputably missing without trace, and these for viruses with subfamilies of estimated ages of 5, 7.8, 14 and 21 Mya.

Anton 'Shrunkâs suggestion, which []he says is based on correspondence with the authors, is that they simply never went to fixation in the human-chimp common ancestor in the first place. '

If ERVs inserted in the germline of common ancestors how have all the traces of all of these disappeared?

Windy 'just to be clear for Willy's and cprs's sake, this is a counterfactual scenario, we share more insertions than that. The paper identifies three types of ERV families: families where no new insertions have occurred after the chimp-human split, families which have orthologues *and* some new insertions in either of the species (indicating that the ERV has been active both before and after speciation), and families which occur only in chimpanzees. As we would expect if the species have recent common ancestry, the non-shared families are a minority.'

The nonshared families are numerically large and reportedly contain numerous orthologous sites in other species (>100 CERV1, most heterologous and ?14 CERV2, based on fig.4's LTR tree http://genomebiology.com/2006/7/6/R51/figure/F4). Do you confidently attribute all this loss to lineage sorting/genetic drift?

This thread's ageing now - but I welcome critical comments.

It seems to me that the only problematic part of the evidence is the estimated age of the ERV's. Otherwise, the observed data is easily explained by independent insertions into the various lines after divergence. As I've said, I don't have any expertise in this area; I don't know if the explanation is as simple as that the estimated ages are just wrong.

cprs,

Given criteria as rigorous, the orthologous CERV 1 and 2 sites for man and orangutan are all indisputably missing without trace, and these for viruses with subfamilies of estimated ages of 5, 7.8, 14 and 21 Mya.

But by those same rigorous criteria, the CERV 1 and 2 inserts arenât found to be orthologous between any of the relevant primate species, and the age estimates are found to be unreliable.

If ERVs inserted in the germline of common ancestors how have all the traces of all of these disappeared?

If the ERVs didnât go to fixation, then by definition they would only have existed in some of our common ancestors. Humans and chimps, after all, are descended from a common ancestral population. If humans donât have those ERVs, it would simply mean that the relevant stretches of our DNA had been inherited from that chunk of the ancestral population which didnât have them either.

But, again, this isnât actually necessary to explain the pattern we see here. It could just be that chimps picked up these ERVs after we split.

The nonshared families are numerically large and reportedly contain numerous orthologous sites in other species (>100 CERV1, most heterologous and ?14 CERV2, based on fig.4's LTR tree http://genomebiology.com/2006/7/6/R51/figure/F4).

I donât think this is correct. The families are large, but according to these papers, none of their insertion sites in different species have been found to be orthologous. Most have been found to be definitely not orthologous (remember, if two sequences are heterologous, theyâre by definition not orthologous!), and the rest probably arenât either, although theyâre more ambiguous.

As shrunk (I think) suggested, I believe you may be misreading this sentence: âConsistent with our findings, the results of a previously published Southern hybridization survey indicated that sequences orthologous to CERV 1/PTERV1 elements are present in the African great apes and old world monkeys but not in Asian apes or humans.â âOrthologousâ is being used here to refer purely to the viral sequences themselves, and not to their insertion sites.

In other words, the sequences in question come from a common ancestral virus, but apes and monkeys havenât all inherited them from an insertion in a common ancestral primate.

Do you confidently attribute all this loss to lineage sorting/genetic drift?

As the others (and the authors themselves) have said, I think it can be attributed primarily to errors in the age estimates they used. If the ERV subfamilies are not as old as the estimates suggest, then nothing ever had to be lost.

Abbie,

I have completed a first pass simulation, based on random ERV insertions*, and wish to build another under a common descent model for comparison purposes.

So I have some questions:

1. Assume that ERV insertions are a random events.
2. Assume the number of successful ERV insertions into an individual from a population during any given time period is proportional to the population of the species. (This makes sense if you think about it. ERVs insertions in question occur during at or near the time of fertilization. It seems reasonable that the number of opportunities for a successful ERV integration is the number of procreation events during a given year, times the probability of the ERV integration.)
3. Assume that the population of each species grows geometrically.

Under these assumptions, you would expect the vast majority of ERVs to be late.

Assuming that the overwhelming majority of ERVs are not in fact late, as evidenced by the calibrated genetic clocks rumored to be as accurate as NIST's caesium based atomic cloks, I assume it is because of near extinction events that cause founder effects.

So, how should such near extinction events be simulated for a fair comparison? At a regular rate, one near extinction per X years, or should these be picked randomly as well?

*It doesn't look good for your side.

Clarification: It seems reasonable that the number successful ERV integrations is the number of procreation events during a given year, times the probability of the ERV integration. The number of procreation events during a given year is probably roughly proportional to the number of individuals in that population.

3. Assume that the population of each species grows geometrically.

For goodness sakes Willy, we were having an interesting discussion here.

*It doesn't look good for your side.

Would that be the side of people who are not clueless about biology? Riddle me this: what's the average time for an ERV to reach fixation in your simulation?

It also seems that WW is completely ignoring the nested hierarchy issue, and focussing on the completely irrelevent issue of whether ERV's are "late" or "early" (whatever the hell that's supposed to mean). This doesn't surprise me. He probably realized, too late, the large number of possible cladograms with only seven species, as his example uses. That number is 10,395. Of course, limiting to just seven species is arbitrary as the ERV pattern is not limited to just those 7 primates. You could even include the Bonobos since, under WW's non-random insertion model there's no reason that chimps and Bonobos should have common ERV's tht indicate common descent. So if he's really being rigorous he should include an 8th species. That bring the number of possible cladograms to 135,135.

IOW, not only is it necessary for WW to explain how a nested hierarchical pattern of any sort can occur without common descent. He also needs to explain how ERV's produce the specific cladogram that is consistent with all other independent lines of evidence.

At the very least, doing all that complicated math should hopefully keep him occupied long enough to allow the grown ups to have an intelligent converstation in peace.

I'm also not sure that WW is correct that ERV's are more likely to occur during fertilization. As I understand it, it only requires that a germ cell infection occur in one of the parents, which could happen at any time. But I could be wrong.

Shrunk,

I think you're misunderstanding something. It turns out that even under a random model of ERV insertions, it is possible to construct a simulation that generates data consistent with the nested hierarchies that support common descent.*

As a comparison simulation, however, I'd like to write a simulation for the common descent model. This will allow a comparison against the non common descent model, to see how significant a difference common descent would make on the outcomes of the simulations.

Late means recent, early means a long time ago.

The argument I am making is a mathematical argument.

If an ERV exists, it is more likely to come into existence when there are more individuals in a population.

Under the assumptions, you would expect most ERVs in any given individual to be late (recent) using evolutionist time scales. Consequently, without some other assumption, you would not necessarily expect nested hierarchies to only support CD. In other words, depending on the probabilities you assign, in a monotonically increasing population, if common ERVs were found across species, you might also find NEs that do not support common descent as well as NEs that do.

Unless near extinction or founder effects cause ERVs to be fixed in the popoulation more quickly. Consequently, under the common descent simulation, I need to somehow account for most ERVs being early, and not late, and also differentiate between ERVs in current individuals versus ERVs established in a population. E.g., maybe ERVs only come into existence during pandemics that decimate the population.

I do not think that scientists believe most ERVs are recent in origin.

Plausible explanations would be founder events and/or near extinctions and/or population boom/bust cycles.

Consequently, I am trying to ascertain what other assumptions I need to make to get a common descent simulation that generates data roughly consistent with actual observations.

Do you understand, yet?

I'm also not sure that WW is correct that ERV's are more likely to occur during fertilization. As I understand it, it only requires that a germ cell infection occur in one of the parents, which could happen at any time. But I could be wrong.

I can go along with that, but the point is that the probability of an RV successfully integrating into a genome times the number of opportunities to do so will give you an expected value. And the number of opportunities is at least in part proportional to the number of hosts in the population. (It is also proportional to the number of RVs in existence at the time, which is itself probably proportional at least in part to the population of the RV's host).

It turns out that even under a random model of ERV insertions, it is possible to construct a simulation that generates data consistent with the nested hierarchies that support common descent

Forget the rest of what you are doing and just focus on this claim. This is the very claim the rest of us are saying is not true, so since you think it is true please demonstrate it.

This is the very claim the rest of us are saying is not true, so since you think it is true please demonstrate it.

In due time. But I think you're disbelief is unfounded, as my claim isn't that hard to believe (unless you're reading much more than what I am writing).

In due time. But I think you're disbelief is unfounded, as my claim isn't that hard to believe (unless you're reading much more than what I am writing).

Taken literally, I agree what you wrote is not difficult to believe: "...even under a random model of ERV insertions it is possible to construct a simulation that generates data consistent with the nested hierarchies that support common descent."

All you would have to do is create a simulation that models evolution and common descent. Such a simultaion can only create a nested hierarchy pattern. Your task, in part, is to show why such a model would not produce a nested hierarchy. Or how a model using non-random insertions and separate creation of species can produce such a pattern.

The "assume geometric growth" line is already enough to trash the whole "model". And Willy, what assumptions are you making about _where ERVs integrate in the genome_?

Stephen Wells,

I haven't even started the common descent model. I am just pointing out that if you assume geometric growth, even 1.0000001, you would expect most of the ERVs to be recent.

Do you disagree with this conclusion?

And, since this conclusion contradicts my understanding of the current observations, this would be a flaw with a model that simply assumed geometric growth. So I am asking about other effects, such as near extinction events, founder events (e.g., due to migration), or other effects that decimate and concentrate ERVs in a population.

Please do try to be honest, Mr. Wells.

But why assume geometric growth? I agree that there will be geometric reproduction rates, but various selective pressures usually relegate population sizes to a quasi-equilibrium. Homo sapiens is currently experiencing geometric growth, true, but that is because we haven't hit the new equilibrium. Historically, even human populations stop geometric growth when they reach the new equilibrium point. What you should be modeling is long periods of no growth with short bursts of geometric growth.

Anton "But by those same rigorous criteria, the CERV 1 and 2 inserts arenât found to be orthologous between any of the relevant primate species, and the age estimates are found to be unreliable."

That's the opposite of what the authors claim, read the paper again.
"Consistent with our findings, the results of a previously published Southern hybridization survey indicated that sequences orthologous to CERV 1/PTERV1 elements are present in the African great apes and old world monkeys but not in Asian apes or humans."
"As was the case for the CERV 1/PTERV1 family, these age estimates are inconsistent with the fact that no CERV 2 orthologues were detected in the sequenced human genome. Again, we were able to detect pre-integration sites at those regions in the human genome orthologous to the CERV 2 insertion sites in chimpanzees, effectively eliminating the possibility that the elements were once present in humans but subsequently excised." The problem is properly acknowledged not brushed away, and they seek to provide some explanations.

There are multiple, rigorously (as rigorous as Windy's well demonstrated findings above) determined orthologues for "chimpanzee, bonobo and gorilla" but "absent in human, orangutan, old world monkeys" for CERV1 and CERV2.

cprs,

You are still misunderstanding the use of the term "orthologous" in this context (for which I think the authors might partially be to blame). It does not mean the ERV's are located at identical sites in African great apes and old world monkeys.

It's the viruses that share the common ancestor. The ERV's are the result of independent infections, much like the ones in the lemurs that started this thread, and as such are not relevent to determining phylogenetic relationships.

You've already been told this. In fact, it's explained in Anton's post that you are responding to.

cprs,

That's the opposite of what the authors claim, read the paper again.

"Consistent with our findings, the results of a previously published Southern hybridization survey indicated that sequences orthologous to CERV 1/PTERV1 elements are present in the African great apes and old world monkeys but not in Asian apes or humans."

Reread that sentence. Theyâre talking about orthologous sequences, not orthologous insertion sites. Thatâs why this was established through Southern blots, which can only tell you whether a DNA sequence is present in the sample, not its actual location. And thatâs why, in the very next sentence, the authors explicitly state that the CERV1 insertions in chimps are not orthologous to those in any other primate:

âThese results suggest that some members of the CERV 1/PTERV1 subfamily entered the chimpanzee genome after the split from humans through exogenous infections from closely related species and subsequently increased in copy number by retrotransposition.â (emphasis mine)

Again: when youâre looking for orthologous sequences, youâre talking about the family tree of the viruses. When youâre looking for orthologous insertion sites, youâre talking about the family tree of the primates. Does that make sense?

The authors say that there is only one line of evidence that these insertions âoughtâ to be orthologous with respect to primates: namely, the results of their age estimator, which is based on sequence divergence. Thatâs the only problem. All other evidence indicates that the insertions are not orthologous, and the authors provide reasons why their age estimator would be in error here. Theyâve resolved the problem, as far as I can see.

But why donât you email them and ask about it?

I see your distinction, Anton, and its validity (it reflects the same misperception I had earlier on with Abbie, but in reverse, if that makes sense, and highlights the plasticity of the term orthologous). Thanks for pointing this out. I am now not sure what the authors actually intended, but you may well be right, and will contact them, since the distinction is important. I hope to post back.

Great, I look forward to their response.

BTW, I don't think "orthologous" is a particularly imprecise term in general. It's just that, in the particular case of horizontal transmission, one suddenly has multiple types of "ancestry" to contend with. I see that the term "xenologous" is sometimes used to denote a common origin through horizontal transmission; using that terminology, the authors might say that the CERV1 family is xenologous across various primate species, but not orthologous across the same. (Unfortunately, "xenologous" doesn't seem to be a very common term.)

W. Kevin Vicklund wrote:

What you should be modeling is long periods of no growth with short bursts of geometric growth.

Thanks. This is exactly the type of feedback I am looking for.

That's Dr Wells to you, little Willy. Have fun with your toy models.

If an ERV exists, it is more likely to come into existence when there are more individuals in a population.

But the fixation rate of neutral mutations is equal to the mutation rate (for ERVs, that would be the probability of integration per individual). So this "most ERVs are late" is just a red herring regardless of whether you are modeling common descent or not.

--

There are multiple, rigorously (as rigorous as Windy's well demonstrated findings above) determined orthologues for "chimpanzee, bonobo and gorilla" but "absent in human, orangutan, old world monkeys" for CERV1 and CERV2.

If they had been "as rigorous" I would have downloaded an example of one of them as well. But the information simply isn't there. As Anton says, the paper seems to use "orthologous" for the virus sequences as well as for their integration sites.

Comments noted Windy, although it may be best to avoid this ambiguity in sense of 'orthologue'. Still no response from the authors so far - none has even read the email yet!

Reply imminent, I'm told.

So here's the question I asked and the answer received this afternoon in full:

cprs: My primary question is about the meaning of the phrase 'orthologous sequences'.

CERV 1/PTERV1
'Consistent with our findings, the results of a previously published Southern hybridization survey indicated that sequences orthologous to CERV 1/PTERV1 elements are present in the African great apes and old world monkeys but not in Asian apes or humans '
The allusion is to another paper on CERV1 which refers to a number of 'ambiguous' orthologues (the vast majority of course being non-orthologous), for which imprecision prevented exact site identification. If the sites were truly orthologous the authors claim at least six of them would have been lost in man and orangutan.

CERV2
'As was the case for the CERV 1/PTERV1 family, these age estimates are inconsistent with the fact that no CERV 2 orthologues were detected in the sequenced human genome. Again, we were able to detect pre-integration sites at those regions in the human genome orthologous to the CERV 2 insertion sites in chimpanzees, effectively eliminating the possibility that the elements were once present in humans but subsequently excised.'

My question is, does the term orthologous sequences refer to identical chromosomal sites presumably inherited from a common ancestor in the primates in whom the sequences were shared (the sense used in the other paper), or does it refer simply to sequences of the same viral origin amongst these primates irrespective of their chromosomal site of insertion? The text seems to point to the former meaning, whilst it's clear that humans lack the virus at the same site as the chimp, after some discussion with others I am now less certain about the other primates who do share the virus (are their insertion sites identical or different from Pan trog.?). Is this perhaps the result of unexpectedly late cross infection?

Author response
In our paper we were referring to both.

In our statement ('Consistent with our findings, the results of a previously published Southern hybridization survey indicated that sequences orthologous to CERV 1/PTERV1 elements are present in the African great apes and old world monkeys but not in Asian apes or humans ') we were referring to sequences of the same viral origin amongst these primates

while in the latter statement (âwe were able to detect pre-integration sites at those regions in the human genome orthologous to the CERV 2 insertion sites in chimpanzees, effectively eliminating the possibility that the elements were once present in humans but subsequently excised.') we were referring to chromosomal sites inherited from a common ancestor in the primates.

The exact origin of these viruses is under investigation.

cprs:
In conclusion, Anton is partly right, but the problematic nature of the lack of CERV2 and possibly 1 orthologues (chromosomal insertion sites) for monophyletic inheritance remains as I last outlined above. The issue is compounded since excision can be excluded and the apparent phylogenetic tree does not match convention. This is not just a question of ERV sequences of common viral origin at least for CERV2, and very possibly in some of the 'ambiguous' CERV1 sites too.

There are many interesting ancillary questions that need to be addressed: Where exactly are these orthologous sites (the authors clearly do know)? How many are shared by other primates, and which? Does this phenomenon also occur for other families of CERVs even if not all are missing, and if so what is the pattern? What about the dating problems - why are apparently old viruses still actively transcribing and also completely absent in two branches of primates? The authors have not yet addressed these directly apart from the paper, although some of them had been raised in my mail.

cprs,

I didn't get a response at all this time. Lucky you!

I'm not sure why you think there remains anything "problematic" here. Anton wasn't "partly right". He was completely right. These ERV's are the result of independent insertions, and the authors' use of the term "orthologous" does not mean the insertions are at identical sites. Humans don't possess CERV 1 or 2 because we were never infected with the corresponding retrovirus. In the case of CERV 1, the molecular basis for humans' resistance to the virus is even known. End of story, as far as I can see.

'We were referring to chromosomal sites inherited from a common ancestor in the primates', but not for man and orangutan. http://genomebiology.com/2006/7/6/R51/figure/F5

cprs,

That figure has nothing to do with chromosomal sites. It's referring to "CERV 2 elements"--that is, sequences of the same viral origin.

I have to agree with, er, Shrunk's agreement with me--the authors have cleared up everything. CERV 1 and 2 sequences across various primate species are orthologous with respect to viral origin, but not with respect to a common primate ancestor.

It's frustrating enough to have to correct creationists' scientific ignorance. It really drives me up the wall when we have to give them remedial lessons in reading comprehension.

cprs:

'We were referring to chromosomal sites inherited from a common ancestor in the primates', but not for man and orangutan.

So you quote from the response you received, then add your own superfluous phrase that has nothing to do with what the authors were writing about? Nice.

Read what the authors said again:

"while in the latter statement (âwe were able to detect pre-integration sites at those regions in the human genome orthologous to the CERV 2 insertion sites in chimpanzees, effectively eliminating the possibility that the elements were once present in humans but subsequently excised.') we were referring to chromosomal sites inherited from a common ancestor in the primates."

They are referring to the intact sites in the human genome that correspond to the sites in the chimp that contained the ERV. That these sites remain intact rules out the possibility that the ERV once existed in the human genome and was subsequently excised. These sites are present in all the primates (humans and orangutans included), which already blows a pretty big hole in the doctrine of denial of common descent.

Anton, fig. 5 refers to CERV 2 and so does the quote. You say 'not with respect to a common primate ancestor', argue with the authors not with me, they say 'inherited from a common ancestor'.

Shrunk, the 'sites' may be present, the ERVs are not, that's the point.

'We were referring to chromosomal sites inherited from a common ancestor in the primates', but not for man and orangutan. http://genomebiology.com/2006/7/6/R51/figure/F5

---facepalm---

Let's break down what they are saying there into digestible chunks. They looked at chromosomal sites that are orthologous, that is, they are inherited from a common ancestor in the primates. But they only looked at those sites in humans and chimps. They didn't look at those sites in gorillas or orangutans or old world monkeys or anything else, just humans and chimps. Therefore, while you can conclude that chimps and gorillas have orthologous CERV 2 sequences, you can't conclude that they have orthologous insertion sites. The authors of the study simply didn't investigate that (possibly because the gorilla data isn't yet available).

There are several possible explanations (and likely the actual explanation is a combination of several) for how this minor discrepancy arose that don't in any way falsify evolutionary theory.

You're still not understanding, cprs.

When they say "inherited from a common ancestor" they are referring to parts of the genome all the primates share in common, because these parts of the genome can be traced back to the common ancestor of all the primates. The quote has nothing to do with CERV 2, except to say that, at the site in the human genome where one would have expected to find the human version of CERV 2 (if CERV 2 arose from a common ancestor of humans and chimps), no ERV is found. This is evidence that CERV 2 was inserted into the chimp lineage after divergence from the human line.

The diagram only shows that the distribution of CERV 2 among the primate lines is consistent with separate, independent insertions, and not with inheritance from a common ancestor.

Shrunk, the 'sites' may be present, the ERVs are not, that's the point.

I have no idea what you think the point is here. Again, this simply indicates that CERV 2 inserted into the chimp line after divergence.

You'll find it easier to understand the article if you don't insist on misinterpreting it to conform to creationist ideology.

cprs,

Anton, fig. 5 refers to CERV 2 and so does the quote.

Sure, but that's irrelevant to the meaning of "orthologous". The word doesn't change its definition for each viral family, you know!

One last time, let's look at what the authors told you.

In our statement ('Consistent with our findings, the results of a previously published Southern hybridization survey indicated that sequences orthologous to CERV 1/PTERV1 elements are present in the African great apes and old world monkeys but not in Asian apes or humans ') we were referring to sequences of the same viral origin amongst these primates

while in the latter statement (âwe were able to detect pre-integration sites at those regions in the human genome orthologous to the CERV 2 insertion sites in chimpanzees, effectively eliminating the possibility that the elements were once present in humans but subsequently excised.') we were referring to chromosomal sites inherited from a common ancestor in the primates.

(my bolds)

For ERVs, there are two meanings of "orthologous." One refers to sequences or elements--the actual genetic sequence of the ERV itself--and this indicates common viral origin. The other refers to sites or regions--the location in the genome of the host primate where the ERV was inserted--and this indicates a common ancestor in the primates.

Both meanings could apply in a discussion about CERV 1, or about CERV 2, or about any viral family. So you can't just look at which family is discussed--you have to see whether the authors are talking about sites or about sequences.

In Figure 5, what are the authors talking about? "Distribution of CERV 2 elements among primates," using PCR and Southern hybridization. This is clearly a discussion of sequences; an element is a DNA sequence, and hybridization can only tell you whether a sequence is present, not where it's located--IOW, it can't tell you the site or region of insertion. So Figure 5 has implications for common viral origin, not for common ancestry among the primate species in question.

Which really shouldn't be surprising. Figure 5 comes from a CERV 2 discussion which is exactly parallel to the CERV 1 section the authors quoted to you--and they did that as an example of the "common viral origin" meaning of "orthologous!

Kevin, wouldn't you be interested in knowing whether ortholgous gorilla sequences have orthologous sites to chimps? There is tentative evidence for some orthologous non human primate sites for CERV1 from the earlier study http://biology.plosjournals.org/archive/1545-7885/3/4/supinfo/10.1371_j…, though the vast majority are not http://biology.plosjournals.org/perlserv/?request=slideshow&type=table&… . Some apparent orthologues on further examination were clearly excluded (macaque to chimp)http://biology.plosjournals.org/archive/1545-7885/3/4/supinfo/10.1371_j…

It will be interesting to see the full data for CERV 1 & 2 when full sequencing is available (no indication from the authors of where the chimp sites were except the index example).

Shrunk, the question is how CERV2 could have extensively populated some primates but not man. If cross infection or autocopying is your only explanation that alone is revealing. Especially if some sites do turn out to be orthologous, since on your current assumptions none of them should be.

Anton, I agree with your points. My intention in linking the figure to the comment was to underscore the complete absence of CERV 2 from oranutans and man, despite its significant presence in other primates ostensibly from the same roots.

I agree it's time to bury the thread (and me) in peace, but I do want to express my appreciation to all for the comments, I've learned a lot from them. I know I'm a bull in a china shop (a medic dealing with the delicate concepts and perhaps sensitivities of molecular biologists). You have a highly enviable field to pursue. Maybe it will be a little grit to the pearl of your thoughts.

Best wishes,
Charles Soper

cprs,

Kevin, wouldn't you be interested in knowing whether ortholgous gorilla sequences have orthologous sites to chimps? There is tentative evidence for some orthologous non human primate sites for CERV1 from the earlier study

That's a rather misleading way of putting it. The authors found strong evidence that various sites (the ones of chimps vs. macaques and gorillas) weren't orthologous, and for the remainder (chimps vs. baboons and macaques vs. baboons), the evidence was ambiguous. Your claim is analogous to, "We don't know exactly who stabbed Julius Caesar and what weapons were used, which is tentative evidence that he was actually killed with a laser gun by a time-traveling Hitler."

Shrunk, the question is how CERV2 could have extensively populated some primates but not man. If cross infection or autocopying is your only explanation that alone is revealing.

Revealing of what? That's what the currently-accepted phylogeny would imply, certainly.

Especially if some sites do turn out to be orthologous, since on your current assumptions none of them should be.

Well, sure--if they turned out to be orthologous, it would suggest that chimps (and bonobos) and gorillas were sister species, which would be pretty remarkable. Not much evidence for that so far, though.

Anton, I agree with your points. My intention in linking the figure to the comment was to underscore the complete absence of CERV 2 from oranutans and man, despite its significant presence in other primates ostensibly from the same roots.

Fair enough, but you incorrectly referred to the insertion site as shared by various primates, but not by orangutans and man--

'We were referring to chromosomal sites inherited from a common ancestor in the primates', but not for man and orangutan

--which simply isn't true. In fact, we know that man does have a site orthologous to the chimpanzee site; that's why the authors were able to examine it and conclude that we'd never had an insertion there!

I have found evidence for a chimp-macaque orthologous site for a non-human CERV, though not as tidy as AS's example above (193), if published I will bring it back here for critical scrutiny.

Dear Abigail, will you please post my message?

Here it is again (I guess a server problem bounced me first time round), orthologues, but so much more needs to be done on this than a paltry and fragmentary search by an outsider, I heartily welcome Prof Eichler's personal commitment to reexamine his data with updated tools.

Charles s: (I presume you are cprs from a year ago)

Several observations:

1) This thread is over a year old, and it's only chance that I saw you post here. If you want to engage in discussion on this topic again, it may behoove you to point out on a recent thread that you have made a comment on an old thread with link to that thread.

2) The example @193 you talk about here and on your blog was given by windy. Proper attribution is important in academia.

3) Word usage: on your blog you used "putative" and "apparent" to describe the anomalous sites. "Putative" is appropriate, but "apparent"" is not. "Possible" or "alleged" would be good substitutes.

4) On a somewhat more recent thread, I calculated the odds that at least one anomalous site per species pair would arise. It is rough, of course, but it came out as about 36%. Follow the link for a more detailed discussion. Bottom line is that the reported results are not at all surprising for so coarse a sample of the genome.

5) Your discussion of what you have found is rather brief. Frankly, I'm not sure what evidence you have found. Could you expand a bit? I'll try to follow this thread for the next while, but be aware that I have some vacation coming up and this thread is not easy to find.

Dr Vicklund, thanks for your comments.
1. I apologise for being slow, although recent comments always show on the main page, whichever thread they appear in.
2. The attribution appears correct given 'Windy's' identity elsewhere.
3. I have changed the description of apparent to potential.
5. I will post the coordinates for the details of the matches, and crosspost to your own blog when it's done. I readily acknowledge they fall far short of the long homologous sequences found for CERV5.
4. I am not fully pursuaded of the applicability of the birthday paradox, not least given evidence of the non random nature of some genetic change (e.g. 1G5 gene mutations in Drosophila and evidence of homoplasy between less 'related' species, giving rise to instances of illusory common descent). Best wishes.

Whoa, full stop!

I am not a doctor, a Ph.D, or anything else like that. The highest degree I hold is a BS in electrical engineering (power systems), unless you want to include the joke degree "Master of Pepology." The closest I've come to a doctorate is that a class assignment of mine has been cited by several doctoral dissertations after it was made part of the curriculum by my professor.

Back to the discussion.

1. I just wanted you to be aware that I and others might miss you posting.

2. If I've parsed what you said correctly, you are accusing Abbie of sock-puppeting on her own blog (ie, that windy is in fact Abbie). This is a pretty serious accusation, at least for the internet. Can you back it up?

3. Thanks!

5. I look forward to it. I have not played with BLAST yet, so while I wait for your results, I'll take a look around so I can better understand your data. I appreciate your willingness to present your evidence with greater detail and explanation. I prefer that over having to guess what someone else is arguing.

4. I think we can both agree that the 'birthday paradox' is, at best, a very rough approximation. In fact, I mentioned some of the reservations I had about it's applicability. The main utility of it is that it provides a base point of reference as to the minimum homoplasy we can expect for a given granularity of the genome. Basically, it establishes that, even with purely random genetic change, evolutionary predicts a certain amount of homoplasy. Obviously, a greater amount of non-random contribution will increase the amount of homoplasy. Now, the important part. If we can quantify the non-random contribution, we should be able to predict the amount of homoplasy. (Of course, keeping in mind that these are statistical predictions). If the predictions match reality, that is strong support for the theory. If it is off, then we need to re-evaluate the theory to see where it is lacking - possibly even abandoning the theory altogether.

Does this make sense to you?

4) On a somewhat more recent thread, I calculated the odds that at least one anomalous site per species pair would arise. It is rough, of course, but it came out as about 36%. Follow the link for a more detailed discussion. Bottom line is that the reported results are not at all surprising for so coarse a sample of the genome.

Just as an FYI, there's an easier way to determine probabilities to find sequences by chance.

I know you said you haven't played with BLAST, but when you do BLAST the sequence, look at the e-value associated. It tells you a probablity that the match happened by chance.

1G5 gene mutations in Drosophila and evidence of homoplasy between less 'related' species, giving rise to instances of illusory common descent).

Do you mean the 1G5 gene mutations as evidenced by a paper by Peter Borger who has yet to be accepted via peer-review to any reputable journal for teh subject of 1G5 gene mutations? The one's who's a member of ISCID, a group who's tagline is "retraining the scientific imagination to see purpose in nature?" The one who's claiming persecution at the hands of Darwinists?

"This is what Kreitman, editor of JME argued as well (Of course he rejected the paper, as did the other five or so Darwin-dominated journals)" and that it's some unnamed mechanism that must be doing it rather than evolution?

The paper the shows he's obviously looking at it backwards, that it wasn't the human, chimpanzee, orangutan, and guinea pig genomes that all had the same mutation, but rather that it was just the rat that had one mutations at each of the sites noted?

Please tell me you didn't really take this "evidence" seriously...

Kemanorel:

Thanks for the heads up. However, I think I was calculating a different probability than the e-value given by BLAST. Also, thanks for the pointer on the paper Charles appears to be referring to. I've now read it.

Charles:

I just read the Borger paper. I hsve a number of comments about it.

Drosophilia spp.

Comparing the introns of the two species reveals ten polymorphic sites immediately adjacent to each other (figure 1, position 153-162). The chance that ten point mutations occur at random in the intron equals 1.4 x 10-18. By way of contrast, the chance that ten adjacent mutations occur in the intron equals 2.2 x 10-14. Because the authors demonstrate no significant deviation from the assumption of a neutral evolution in this region, natural selection cannot explain this cluster of mutations. It is therefore reasonable to assume that the cluster of mutations observed in the introns was not the result of a random accumulation of (point) mutations.

What Borger fails to consider is that point mutations are not the only source of mutation. My guess is that this is the result of the DNA repair mechanism. Ie, that a break in the DNA occured and was repaired with a short, random sequence. Not the only explanation of course. But the most parsimonious.

the sequences were obtained from species
inhabiting separated continents and are therefore reproductively isolated.

Borger is wrong. There is no indication that these populations have been reproductively isolated for a sufficiently long preiod of time for these mutations to arise in isolation. Both of these species are native to Africa. In most of the locations supplying the genetic samples, Drosophilia is an invasive species. Any isolation based on current geographic location is only a few hundred years old, at best, significantly less time than the original paper Borger refers to calculates. This means that a single isolated population might have colonized several different continents, while another population might have populated other areas of those same continents.

If there was no additional information for the 1G5 genes, we would most probably be inclined to argue that D. mel-1, -4, -5, -6, -11 and -13 are very closely related, since they all have exactly the same gene and thus have a very recent common ancestor. Likewise, D. mel-7, -9 and -12 must have a recent common ancestor as they have several shared point mutation; for the same reason D. mel-3 and -10 must share a recent common ancestor.

The information he was lacking (I hope for his sake) puts the random mutation hypothesis back on solid ground. Also note that the authors of the original paper did not claim these populations were isolated. I will note that the authors of the original paper treated the ten contiguous changes as separate point mutations, so they may have overestimated the amount of intronic variation.

Conclusion: Borger's failure to allow for other types of mutation and lack of knowledge about the chrono-geographic location of the population of Drosophilia renders his argument worthless.

Vitamin C

As Kemanorel noted, Borger is assuming that the rat gene has not had any mutations, instead treating it as if it were the ancestral gene. Once you recognize that the rat gene can also experience mutation, the phylogeny puts the great apes as closely related to humans, and rats and guinea pigs as distantly related on a different branch.

Conclusion: Not enough data to support an inference of non-random mutation (wrt location in genome) - you really need a more diverse sample (breadth and depth). That said, the concept of genomic hotspots is not inconsistent with evolutionary theory. There is almost certainly a non-random component to the location of mutations which has long been recognized.

If I've parsed what you said correctly, you are accusing Abbie of sock-puppeting on her own blog (ie, that windy is in fact Abbie)

LOL!

**shrug**

Sorry for the honorary doctorate, Kevin, I confused you with Stephen Wells.
I note the criticisms of Borger's paper with interest - well sleuthed.
As to the sock puppeting, I don't at all agree it's such a serious matter - even Christ once concealed his identity - and why should Abbie be seen to demean herself to deal personally with every tedious objector?
Apologies too for my snail-like pace - I have been busy of late, will post (and cross post) details soon, it's simply a matter of fishing through my messy data storage - today if possible, the findings are modest - sifting through the genome and observing its bizarre patterns of repetition has been fascinating to me as a novice, but I appreciate much better some of the difficulties.

I searched for the pol gene of CERV1 (4544..5611 from NCBI's AY692036.1) in the macaque genome and then took contiguous sequences of the hits from this with adjacent non CERV containing sequence and blasted it against Pan Trog.
In the macaque contig NW_001112574.1 the a portion of CERV1 pol gene is found at 7352782-7351802(-), (though there's a gap in pol sequence from its 487th to 664th nucleotide).
Two non CERV containing adjacent fragments (I called a and b) from the macaque contig are also with the pol gene in the chimp contig for chromosome 2, Contig33.125 (AACZ03012828.1).
The fragments a and b are found at 7347266-7347577 and 7349461-7349794 in NW_001112574.1. None of 94 other chimp contigs shared either of these two non-CERV fragments from the macaque genome and CERV1 pol sequence.
A third non CERV fragment from the same macaque contig (which I called c) 7346538-7350059, near the pol sequence, was not in the chimp contig, but showed widespread distribution throughout the genome of several primates (nearly 3 k hits in man and 3,048 in orangutan). It was inside the regions of 15 different macaque genes.

The second interesting site was shared between the gorilla contig CABD02426596.1 and chimp AADA01328632.1 . Most of the shared sequence is from CERV1, but there is a non CERV1 region from 6129 to 6395 in the gorilla sequence also found in the chimp sequence at 800 to 1065 (Blast scores: 375 375 100% 3e-107 92%).

Comments?

Sorry... just got back last night from New Orleans and a cruise in the Caribbean, prior to which I had my usual vacation and was working massive overtime. In short, I haven't had much of a chance yet to look at your results in detail, plus my computer doesn't seem to play well with the BLAST website, so it's been a slog. And it always takes several days to recover from a long trip. So, probably no comment until next week.

Hmm... maybe if you told me the parameters you used it would go faster?

No hurry, I've been much slower, and as I say I fully agree they're hardly earth-shattering findings. If you need help with the parameters please email me cpsoper at gmail. I have saved some but not all the search strategies and can send them on.

Still no thoughts?

I've pretty much had to give up on this until I get a new computer.

Kevin, if you (or others) get a chance to look at this or other apparent discrepancies, I'd be grateful for a mail.