Retroviral promoters in the human genome
|August 22, 2008||Posted by Dave S. under Intelligent Design|
The paper whose abstract lies below the fold has been cited as supportive of intelligent design here by my friend Casey Luskin of the Discovery Institute . I’m afraid I disagree with Casey’s analysis but I don’t have access to the full paper and would welcome review of my take on it from someone with access and expertise in virology. I’ve never agreed that ID, per se, predicts that “junk DNA” isn’t really junk. That’s a prediction based on young earth creationism. If an omnipotent designer created a perfect human genome 6,000 years ago then we might reasonably expect most of it today would still be functional. Design detection in and of itself does not predict any specific state of perfection or decay in the design. Thus the common assertion that “ID” predicts junk DNA will have function is not strictly an ID prediction at all but rather a young earth creation science prediction. Failure to make the origin of the predictions clear in these cases is a big reason why we keep getting slapped down in courts. It’s too transparent that design detection alone doesn’t predict things about junk DNA. You have to add in some young earth creationism to get there.
Retroviral promoters in the human genome
Andrew B. Conley , Jittima Piriyapongsa and I. King Jordan
School of Biology, Georgia Institute of Technology, 310 Ferst Drive, Atlanta, GA 30306, USA
Motivation: Endogenous retrovirus (ERV) elements have been shown to contribute promoter sequences that can initiate transcription of adjacent human genes. However, the extent to which retroviral sequences initiate transcription within the human genome is currently unknown. We analyzed genome sequence and high-throughput expression data to systematically evaluate the presence of retroviral promoters in the human genome.
Results: We report the existence of 51,197 ERV-derived promoter sequences that initiate transcription within the human genome, including 1743 cases where transcription is initiated from ERV sequences that are located in gene proximal promoter or 5′ untranslated regions (UTRs). A total of 114 of the ERV-derived transcription start sites can be demonstrated to drive transcription of 97 human genes, producing chimeric transcripts that are initiated within ERV long terminal repeat (LTR) sequences and read-through into known gene sequences. ERV promoters drive tissue-specific and lineage-specific patterns of gene expression and contribute to expression divergence between paralogs. These data illustrate the potential of retroviral sequences to regulate human transcription on a large scale consistent with a substantial effect of ERVs on the function and evolution of the human genome.
First of all one must understand that retroviruses all incorporate a promoter region. They must. Their modus operandi in reproduction is to commandeer the DNA transcription machinery in a host cell so that it manufactures copies of the viral particle. Basically the virus uses reverse transcriptase to insert a copy of its own code into the host DNA. The insertion includes a so-called “promoter region” which causes the victimized cell to execute the foreign instructions.
Sometimes the viral promoter region will also promote adjacent non-foreign code to be transcribed as well as the foreign code. Indeed, this is a big problem for “gene therapy” in medicine. In one method of gene therapy an engineered retrovirus is used to deliver a good copy of a defective gene (along with a promoter region) into the DNA of someone with a genetic disease. As of yet, unfortunately, the insertion point of the good gene cannot be controlled and this lack of control sometimes results in very undesirable side effects. The most common undesirable side effect AFAIK is cancer.
So the way I read the referenced paper is that it simply identified 114 ERV promoter regions in the human genome which happen to be promoting a non-foreign human gene. Given that it was only 114 out of nearly 60,000 ERV promoter cites this doesn’t seem to have any bearing on intelligent design but is merely a predictable consequence of so many ERV promoters embedded in the genome. Some of these 114 may actually have some beneficial effect but that’s doubtful as random changes in finely tuned machines rarely have any benefit. I think it’s more a matter of these 114 not having any really negative effect which makes them invisible to natural selection and thus they can persist in the genome. If there are a larger number of these among the 60,000 ERV promoter regions I don’t find that something that should be unexpected. After all, the human genes these ERV promoters are promoting obviously have some purpose else they wouldn’t be human genes in the first place. These genes must have had their own native promoters at some time in the past and it may simply be that the ERV promoter made the original promoter redundant.
I don’t see at all how this either supports or detracts from the intelligent design hypothesis. The only way I’ve ever seen the existence of retroviruses as supportive of intelligent design is to propose them as a good candidate for a tool that a hypothetical designer could use to effect evolutionary change. A highly infectious airborne or waterborne retrovirus that targets a specific species could insert heritable genetic material into the germ line of that species. The inserted material could cause any kind of change in the species the designer desired including saltation into a new species. As our own abilities as “intelligent designers” increases we’ll likely be altering the course of evolution ourselves in this manner. Obviously it doesn’t require anywhere near omnipotence to effectively accomplish any wholesale tinkering with the evolution of life.