WEIRD COOL EXPERIMENT ALERT!
For some reason, I have no idea why (Im sure they have a good reason-- obesity research, farming research), scientists were playing a selection game with chickens.
Select the skinniest chickens. Breed them. Select the skinniest chickens. Repeat.
Select the fattest chickens. Breed them. Select the fattest chickens. Repeat.
Keep doing that until you get a population of skinny chickies and another population of fat chickies. How are these two populations different?
Well, there was clearly a behavioral difference between these two. Fat chickens were compulsive eaters, while 2-20% of the skinny chickens, even if they were given all the food they wanted, died from anorexia.
So scientists did what any rational person would do: They ground up the chicken brains and looked for gene expression differences.
Guess what one of the big differences was.
Guess.
Youll never guess.
ERVs!!!!
Skinny chickens? They had increased expression and increased copy numbers of a still active ERV in chickens, avian leukosis virus subgroup-E.
At first, this didnt totally surprise me. The starving chickens are under stress. Their DNA is not being epigenetically modified properly, because the food isnt there to get the parts the cell needs to do it. No epigenetic silencing, ERVs are free to be active. Their host is under stress. They need to jump ship.
So, active ERVs in skinny chickens is an effect of skinniness, not a cause... BUT, the researchers looked at other families of ERVs in chickens. Only the ALV-E ERVs changed their expression/copy numbers! Not other ERVs, not other subtypes of ALV (A/B/C/D/J). If this was a global effect of epigenetic modifications, all the ERVs would have started acting up, right?
No idea what this means yet. Dont run around telling your friends "Dont eat your veggies so your ERVs act up and you can get all skinny!!!" Just file it under 'weird cool experiment' for now :)
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If ERV activation is due to stress, wouldn't you expect the ERVs to be activated in the overeating population and not the starved one? After all overeating->increased oxidative stress (see al the brouhaha about the calorie restricted monkeys).
I prefer the hypothesis that active ERVs are getting inherited along with loci that increase overeating. Perhaps the whole region is epigenetically activated, and inherited like a big epiallele. But why only one type of ERV?
Not sure how amenable chickens are to genetic manipulation, but it would interesting to see what happens if you add in more copies of the ERV into wild-type chickens (maybe under a constitutively active promoter). I suppose an easier experiment would be to simply intentionally starve the chickens and see if ERV expression increased. Either way it would allow you to work out the causal relationship.
So, ERV, did Ian Musgrave set you onto this topic too??
We have enough puppets.
Tell you what.
Go do some of your original so-called "research"
instead of reporting what's already known.
Yawn.
@philios
Wtf? EVR is a science blogger so she blogs about really interesting science. She is doing her own research, and looking at other people, and telling us interesting stuff about what she looks at.
(also I'm confused about why such a strong reaction to chicken ERV papers. I mean vaccinations and evolution i can understand...but this is gene expression in chickens. Am I missing something?)
Lab Rat:
phobos is probably a Kwok meat puppet. Earlier this week, Kwok falsely claimed on The Intersection that Abbie refuses to acknowledge Ian Musgrave's contribution to her takedown of Behe.
(further background: Abbie kicked John Kwok off her blog for weird stalking behavior and he's been on the attack ever since)
I wonder what kind of genetic diversity they had in the populations. I mean if for some reason one of the skinny chickens had a preexisting tendency towards ALV-E, or if the ERV is near some other "skinny gene" then they could have unknowingly been breeding the tendency as well as the skinny trait.
This is interesting but I'm skeptical that it will tell us much about anorexia in humans given that anorexia is to a large extent a culturally mediated disease.
Umm... I'm less interested in what this has to tell us about anorexia and more interested in what this is telling us about a freaking ERV changing behavior! While I'm skeptical the extent that they affect behavior I think that it is defiantly worth looking into.
#3:
What the heck are you on about?
philos is an HIV-1 Denier from Old ERV. He leaves the same comment over and over, but this ones actually kind of fun, just for the random Ian reference.
mikka-- Epigenetic modifications need food. Like how pregnant women are supposed to take folic acid sups to prevent some birth defects? Starvation leads to altered epigenetic modifications-->ERV activation.
Others-- FOR REAL! Viruses are CHANGING your MIND! BWAHAHAHAHAHAHAHA!
I'm in the epi-phenomenon camp (until proven otherwise). All sorts of genetic peculiarities will come about when you have a severe population bottle neck. It's where genetic drift becomes huge.
And you would expect relative weight to be affected by so so so many genes affecting so so so many diverse processes. (People affected by the flu virus lose weight, too.) Which means that even if a link between these ERVs and weight gain can be shown in this chicken population, it's not necessarily evidence that this provides useful insights into normal eating behavior or the "normal" disorders (in chickens or any other species).
So I'm not yet ready to concede that "ERVs roolz da bodiez".
Chickens can really be anorexic? I've always assumed that was unique to our own species.
My head is like that guy on the Scattergories box.
neat! thanks for sharing