Casey Luskin is evidently unaware of this series, as he managed to smack his loverly, loverly face into a couple of them in his recent
blog post ‘news release’ at Evolution News & Views (Why is EN&V indexed by Google News, again?).
Casey TARD: ID proponents would predict function for ERVs… As William Dembski wrote in 1998, “If, on the other hand, organisms are designed, we expect DNA, as much as possible, to exhibit function.”
Casey is referring to a recently published paper, Retroviral promoters in the human genome, where they sifted through the human genome for potentially active ERV ‘LTRs’, and they found some. YAY! COOL!
But Casey thinks that means ERVs are ‘functional’.
I dont think Casey knows what ERVs are.
If Ive said it once, Ive said it 1,000 times– You do not want ERVs to be functional. Functional ERVs would be ‘endogenous proviruses’, thus they could kill you. Even though the most ‘popular’ retrovirus, HIV-1, doesnt cause cancer, cancer is retroviruses favorite trick! B-cell leukemias, T-cell lymphomas, erythroleukemia, myeloid leukemias, osteosarcomas, fibrosarcomas, carcinomas…
No one, including cdesign proponentsists, want ERVs to be functional!
What we do know, and have known since at least 1990 (thats pre-cdesign proponentsists, Casey) is that components of ERVs can be co-opted, through evolution, to perform other tasks. ‘LTRs’ are the promoters for retroviruses (I havent gotten to them in the ‘Intro to ERVs’ series yet). Its possible that a retrovirus plops down next to a gene, and the genes like ‘Whoa! Ur a better promoter! I keepsies you!! *hug*’ Its also possible that a retrovirus plops down next to a gene, and the gene says ‘Piss off.’ Its also possible that a retrovirus plops down next to an oncogene, and the cell cant turn off the viral promoter… YAY CANCER!
While we have been finding functional ERV promoters here and there (because they cause a disease, we notice them), no one has ever done a genome wide screen for LTRs that have been domesticated for ‘normal’ use by our cells. So Conley & Crew used a couple of cool new genetics tricks to determine just how many ERV LTRs have the potential to act as promoters. They found ~100 genes that were probably ERV-promoter-driven, and lots that might have ERV promoters as ‘alternate’ promoters.
They also did a fun experiment with broad-reaching implications– Test for ERV-driven transcription differences in human vs mouse tissue. They used ‘GSTO1‘, a gene with ERV promoters upstream, and has also been associated with ‘cerebrovascular diseases including Alzheimer’s disease, Parkinson’s disease, vascular dementia and stroke.’ Mice dont have an ERV north of GSTO1. Mice and humans both have GSTO2, and neither of us has an ERV north of that gene.
Mice and humans have similar transcription levels of GSTO2.
Mice and humans have different transcription levels of GSTO1, in part because our GSTO1 transcription uses an ERV promoter instead of the ‘normal’ one! This little exercise just demonstrated one of the reasons humans are different from mice (well, not just humans, all primates have this ERV insertion).
And think about what it leads towards– Not only elucidating the teeny-tiny-differences that lead to speciation events, but what makes a breast cancer different from regular breast tissue? What makes a brain with Alzheimers different from a normal brain? We know there are transcript differences, but are the diseases caused by an alternate transcript initiated by an ERV promoter? Is it a loss of control of that ERV promoter that leads to disease? Can we give people therapies (ie epigenetic modifiers) to control wayward ERVs induced transcription?
This paper also does a great job of emphasizing the huge role retroviruses have played in the evolution of life on this planet:
The lineage-specific regulatory effects of ERV promoters can be attributed to the fact that ERV sequences result from past germline infections, many of which occurred relatively recently along specific evolutionary lineages. In fact, most of the ERV sequences in the human genome are primate-specific (Sverdlov, 2000), while most human genes are far more ancient and share orthologs with distantly related species (Lander et al., 2001). This means that regulatory effects exerted by ERV promoters will often lead to expression differences between primate and non-primate orthologs or between deeper evolutionary lineages for more ancient ERVs. In other words, ERV promoters are likely to drive evolutionary changes in gene expression, long thought to be an important determinant of species divergence (King et al., 1975).
Of course, to Caseys lovery, loverly ears, the authors are just ‘pandering to the evilutionary para-dig-um’. lol.