ERVs, Epigenetics, and Testicular Cancer

Once again, ERVs, the best goddamn workhorse in the stable, have provided another great example for explaining How the World Works. This time? How a functional ERV protein interacts with normal cellular proteins to cause epigenetic changes that lead to cancer:

Human Endogenous Retrovirus Protein Rec interacts with the Testicular Zinc Finger Protein and Androgen Receptor.

WARBLEGARBLE!!! FUNCTIONAL ERVs!

WARBLEGARBLE!!! EPIGENETICS!

EVERYTHING YOUVE BEEN TOLD ABOUT EVILUTION IS WRONG!

JESUS IS LORD!

heh.

That title/abstract looks scary (okay, it is scary. there is a reason I didnt go into cell bio), but the basic premise of the paper is super easy and really cool.

You all know the basic parts of any retrovirus, endogenous or exogenous, are gag, pol, env, and LTRs. There are also lots of accessories retroviruses can add-- one of which is 'rec' (rec has other names in other retroviruses, rex, rev, etc). Know how retroviruses like to make one/few RNA or proteins, and chop them up into lots of little functional RNA/proteins? Rec and its genetic relatives help transport RNA right out of the nucleus so it doesnt get chopped up (the not chopped up RNA makes a different protein).

Its complicated, but retroviruses can only get so long, so they have to get as much bang out of their buck as they can.

Now, while the vast, vast majority of ERVs in your genome are just solo LTRs or degraded segments of used-to-be genes, there are a few that can still code for functional proteins. We still have a Rec protein that works from the HERV-K family ERVs (the youngest family).

This functional Rec is not a sign sent from Jesus, telling us that he loves us.

It causes cancer.

Ball cancer.

This functional Rec wanders around and interacts with Testicular Zinc Finger Protein (TZFP). TZFP is a transcriptional repressor-- tells the transcription machinery "DO NOT MAKE THIS SHIT!!" It does this via epigenetics.

**GASP!!**

The 'magic' of this epigenetic modification, is that TZFP binds to activated Androgen Receptor (transcription factor) and recruits Histone deacetylase 2, an epigenetic silencer that makes modifications to the histone bound specific bits of DNA with "DO NOT MAKE THIS SHIT!!" flags.

When this endogenous Rec binds up TZFP, you have too much activated Androgen Receptor hanging out. Androgen Receptor is an oncogene if you have too much of it because it starts telling your cells to make stuff its not supposed to make. In other words, cancer.

Fantastic.

So next time a Creationist tries to use functional ERVs or Epigenetics as evidences of Creation, look them square in the eye and say:

Ball cancer.

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Hey, you guys remember a while back, when Casey 'Tits' Luskin about peed his pants because 'ERVS AR BE FUNKSHUNAL!!' Except, this is really another case of Creationists not knowing the difference between an ERV, solo LTRs, and random wayward ERV genes. And those solo LTRs that could theoretically…
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<finger my testicles joke goes here>

I've heard of getting a finger wag at the doctor's office, but I thought it went somewhere else...

But "junk" DNA has a use that means GOD!!!!!11!1!!!one The use is to kill you slowly and painfully but it prooves GOD loves us and wants us to come home... as slowly and painfully as possible.

By the backpacker (not verified) on 30 Mar 2010 #permalink

"Testicular zinc finger protein" would be an excellent name for a rock band.

By Ktesibios (not verified) on 31 Mar 2010 #permalink

It's a great study, actually, and I'm glad you pointed that out. Another piece of evidence that viruses - even ERVs - can mess with the epigenome. And just like in alot of the other cases being discovered, the end result is cancer.

By ArchTeryx (not verified) on 01 Apr 2010 #permalink

What is sad to me is that this thread has failed to provide any creationist amusement. Just the usual "Darwinoids".

Damn it, as a "Darwinist", I demand satisfaction.

Where is Casey Lus(tits)kin when you "need" (I really "need" him) him here?

pretty sweet stuff! zebrafish ball cancer happens to be my area of research.