Endogenous Retroviruses in the Case for Common Ancestry
|May 10, 2007||Posted by Dave S. under Biology, Evolution, Intelligent Design|
We often hear the argument that evidence for common ancestry can also be interpreted as evidence of common design. Some years ago I made the argument that there was no way to discriminate between the two. The argument was countered (successfully IMO) by endogenous retroviruses (ERVs).
A bit of background about ERVs. Retroviruses replicate themselves by invading a host cell and inserting a package of viral genes into the host DNA along with promoters that cause the cell to express (translate and manufacture into proteins) those genes. The expression of those genes makes new virus particles and can compromise or kill the host cell in the process. The active viral gene package, after insertion, is called a provirus. Proviruses can be deactivated by a number of means becoming inert and leaving just the mostly intact but non-functional genes still in the host cell genome. Occasionally a germ cell can become infected and if it survives to become a new organism the deactivated provirus becomes what’s called an endogenous retrovirus (ERV for short) and gets passed along from parent to offspring down the lineage. Because the ERV serves no function it is not conserved by natural selection and is slowly mutilated by random mutations over millions of years until it is no longer recognizable as the strain of provirus it once was. There may be preferred insertion points in the genome for the RV genes but if there are there are a great many potential insertion points.
The case for common ancestry is made by finding the same strain of ERV inserted at the same place (loci) in the genomes of closely related species such as different primate species. The argument is that the RV infected a germ cell in a common ancestor and the ERV was then inherited by all the descendents. When the species splits or spawns a new species that is reproductively isolated each species has the ERV but, and here’s the key, random mutation changes each ERV differently. By comparing the differences in ERV sequences at the same loci in different species one can establish a rough date for the original infection in a common ancestor given a more or less average background rate of random mutation.
ERVs in various levels of decomposition make up some 8% of the human genome. Occasionally however an ERV is conscripted for some useful purpose and is conserved. It should be noted that human designers use domesticated RVs as delivery vehicles to insert foreign genes into genomes to create so-called GM (genetically modified) organisms like tomatoes with longer shelf lives and whatnot. Theoretically this can be used to distribute vaccines for various diseases. A GM banana for instance could carry genes that cause it to manufacture a vaccine for malaria. Eat a GM banana and you’re immunized against malaria. More significant to the case for intelligent design is that this is a mechanism a designer could use to modify genomes – introduce a virus into the population which inserts genes that cause the spawning of a new species. So if anyone asks about possible mechanisms a hypothetical designer could use to intervene and direct evolution that’s a good answer. Human designers are already doing it so it’s a proven mechanism. Morever a highly infectious retrovirus inserting genes that cause modification and speciation could convert entire populations into a new species in just one or several generations and at the same time cause the original species to become extinct virtually overnight. That fits wonderfully with the indisputable testimony of the fossil record which paints a picture of abrupt speciation, millions of years of little if any change in the new species, followed by an abrupt extinction. A mechanism for causing saltation of new species is thus shown.
Anyhow, back to the case for common ancestry. Recently in a private forum where others are concerned with intelligent design I brought up the case of ERVs as evidence supporting common ancestry vs. common design. If common design instead of common ancestry the designer is evidently using existing species in situ as the template for new species. If that’s the case there’s effectively no difference whatsoever between common design and common ancestry.
An objection was raised about how it was possible for a germ cell to become infected by an RV in the first place and secondly how could it survive the infection and go on to grow into a reproducing adult. As it turns out it probably isn’t very likely at all for sperm cells to be either infected with a provirus or survive the infection. Sperm are created and grow quickly into mature cells with a lifetime measured in days. Once mature they are stored behind a blood barrier which inhibits viral infection. They are also very active cells and even if infected would likely be hobbled enough to not be successful at fertilizing an egg. Egg cells however are a whole different story. In mammals a female is born with a lifetime supply of primary oocytes (immature egg cells) already created. There is also no blood barrier where they are stored in ovarian follicles. They are stored in a state of suspended animation or dormancy. Upon their creation in the developing embryo meiosis is halted in the first of two meiotic divisions at anaphase (IIRC) while still diploid (full compliment of 46 chromosomes). DNA replication and segregation into haploid germ cells is not completed until, beginning with puberty, one or a few resume meiosis and become mature egg cells ready to be fertilized. Thus a primary oocyte can hang around in a dormant state for 50 or more years and ostensibly be infected by an RV at any time. Because they are dormant gene expression is suppressed and even after a provirus is inserted into their DNA it isn’t likely to be expressed. The provirus remains dormant as well in other words. Because meoisis hasn’t progressed very far there is still a lot of DNA replication and shuffling (segregation and crossover) that goes on before the egg is mature. My conjecture is that the provirus is deactivated or very likely to be deactivated during the completion of meiosis (possibly from either segregation or crossover) so it is converted at once from provirus to endogenous retrovirus without ever having an opportunity to be expressed into new virus particles. This would handily explain how so many ERVs have found their way into primate genomes.