So I got the idea to do this after stumbling across a bunch of viral/farmyard stories this week. I know its currently Tuesday, not Sunday, so, SURPRISE!!! BARNYARD WEEK!

If you ERV readers are anything like me, you have spent countless nights tossing and turning in bed, unable to sleep, unable to stop pondering one of lifes greatest mysteries:

Why are some chickens white?

I finally accepted the fact that this question was ultimately unanswerable, like “What is the meaning of life?” or “Why did anyone ever think Jim Carrey was funny?”. Then I found out that the question actually had an answer. They figured it out like 5 years ago. Its because of an ERV.

Complete association between a retroviral insertion in the tyrosinase gene and the recessive white mutation in chickens.

Quantitative effects of an intronic retroviral insertion on the transcription of the tyrosinase gene in recessive white chickens

Now, Im talking about just plain white chickens, here. A recessive phenotype in numerous breeds of chicken. Not chickens that are normally white (dominant white alleles). Not the albino ones with pink eyes, just white chickens with normal pigmented eyes, when lots of their brothers and sisters are brown/black/red.

Albino chickens are white because they have a tiny deletion in their tyrosinase gene. Tyrosinase is an enzyme that helps make melanin pigments like eumelanin and phaeomelanin which color skin/fur/feathers. Deletion = no TYR = no pigment = albino chicken.

Something different is going on in the white chickens. Sure, theyre white, but their eyes are still pigmented normally. It cant be an overall defect in the TYR gene, like the albino chickens.

When scientists investigated the differences between Wild-Type chicken TYR, and white chicken TYR, they didnt see any differences in the TYR messenger RNA. Everything looked the same. So there definitely wasnt anything wrong with the message, like what was going on in the albino chickens.

But they did find a difference between the TYR genes in WT and white chickens… Apparently in white chickens, there is a HUUUUUUUUUUUUUGE insertion in the TYR gene. 7,700 bp virus, Avian Leukosis Virus, plopped its little virus butt into intron 4.

Its in an intron. Introns get chopped out of the mRNA as it moves from the nucleus to the cytoplasm to the ribosomes to make the protein. There is an initial difference between the WT and white chicken TYR mRNA, but that difference goes away, so the TYR protein works fine.

So… if the insertion is in an intron, and the message is fine, and the final protein is fine… Why are the chickens white? And why are their eyes still pigmented just fine?

While the TYR message and protein are fine in white chickens, that big ERV in the intron still comes at a ‘cost’. Not only is it ‘harder’ to make such a large RNA that is just going to go to waste, long-time readers of ERV know that your genome goes to extreme lengths to silence ERVs. Thus, again, even though the ultimate message and protein are fine, white chickens do not make as much TYR mRNA as their WT counterparts, and are therefore white. And while the message can come out fine, sometimes the RNA polymerase just gives up, and the TYR mRNA is made without the last exon, #5, so the mRNA cant make a normal TYR protein.

This suppression is not so severe in the chickens eyes. Why? … They dunno :-/ But they proposed a hypothesis:

Thus, we propose that transcription of the tyrosinase gene is controlled by a different regulation mechanism in the retina than in the skin.

No experimental support for this, but its theoretically a valid hypothesis. Maybe a ‘more aggressive’ set of proteins initiating transcription could overcome the burden of the retrovirus in the intron.

But now we can all sleep soundly at night. We know why some chickens are white.

Comments

  1. #1 Mu
    May 24, 2011

    Damn you, I just solved the “why the chicken crossed the road” problem. Now I have to start over to account for chicken ervs as confounding factors. Four years and 10 million in federal grants down the drain.

  2. #2 Pete D
    May 24, 2011

    As long as they still taste the same. Dude, how can you not watch the Jimmy Tango’s Fatbusters skit from SNL and not think Carrey was funny in that?

  3. #3 Sili
    May 24, 2011

    If you ERV readers are anything like me, you have spent countless nights tossing and turning in bed, unable to sleep, unable to stop pondering one of lifes greatest mysteries:

    No, but I did just spend an hour listening to The Muppets on Youtube.

  4. #4 Sili
    May 24, 2011

    This suppression is not so severe in the chickens eyes. Why? … They dunno :-/ But they proposed a hypothesis:

    Well, I can see how eyes that are overly sensitive to light might be selected against.

  5. #5 jose
    May 24, 2011

    Thank you ERV. I’m using this post to introduce my little cousin into the world of antipanadaptationist heterodoxy. He likes chickens.

  6. #6 daedalus2u
    May 24, 2011

    My guess is that the cells in the retina hang around for a lot longer than the cells that make feathers, so a reduced amount of tyrosinase can still make enough melanin if it works at it longer.

  7. #7 Emerson White
    May 24, 2011

    Feathers grow very rapidly, so they have to lay down pigments in a real hurry, if the enzymes are slow to produce but function at a normal rate they probably just miss their window of opportunity, where as the new cells of the iris and the exposed skin have plenty of time to develop color. That is my stab in the dark. Counter evidence to this might be the white skin, but I think most breeds have white skin under their feathers.

  8. #8 Emerson White
    May 24, 2011

    Goddamnit! Daedalus totally beat me by one minute because I took the time to type it out longer! Grrraaaarrr!

  9. #9 daedalus2u
    May 25, 2011

    This is interesting. I would bet that this mutation confers some resistance to melanoma.

  10. #10 theshortearedowl
    May 25, 2011

    My bet is on a splicing issue – pigmentation in eyes vs. skin/feathers has something to do with the exon(s) beyond the 4th intron – either differential expression or accumulation, or just the presence of the correct substrate in those tissues.

    To clarify: I doubt many/any full-length proteins are produced after an insert of that size; maybe the pigmentation effects in the eyes can be produced by shorter versions of the gene, but the pigmentation in the skin/feathers needs the long version.

  11. #11 theshortearedowl
    May 25, 2011

    This is interesting. I would bet that this mutation confers some resistance to melanoma.

    What’s your reasoning? Generally, less pigment means less protection against UV light, and so greater risk of melanoma.

  12. #12 daedalus2u
    May 25, 2011

    Melanoma are characterized by high production of melanin. Inhibiting melanin production is an anti-melanoma treatment.

    The protection would be downstream of a mutation that causes melanoma. I have no idea if chickens get melanoma.

  13. #13 theshortearedowl
    May 27, 2011

    Characterised by, yes (although not in all cases). Caused by, no. Pale-skinned people who don’t tan easily are at increased risk of melanoma because they produce less melanin. (I am reasonably certain this also applies to chickens.)

    Melanomas may be treated with melanin-inhibition because the melanin renders them resistant to some anti-cancer treatments.
    http://www.ncbi.nlm.nih.gov/pubmed/21542806

  14. #14 daedalus2u
    May 27, 2011

    There is the production of mitogens when melanin is produced. My thinking was that those mitogens are important in the rapid growth of melanoma. If the ability to produce melanin was stunted, so would be the production of mitogens by that pathway and (maybe) the growth rate of melanomas would be stunted too.

  15. #15 fnxtr
    May 29, 2011

    So… I was looking at the ERV primer posts from a while back and wondering, do randomly-inserted LTR’s ever promote junk? Like, trigger production of useless proteins the cell doesn’t know what to do with?