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DNA and Insertions: ERVs

"The new DNA evidence has a very important role beyond illuminating the process of evolution. It could be decisive in the ongoing struggle over the teaching of evolution in schools and the acceptance of evolution in society at large. It is beyond ironic to ask juries to rely on human genetic variation and DNA evidence in determining the life and liberty of suspects, but to neglect or to undermine the teaching of the basic principles upon which such evidence, and all of biology, is founded." 

~ Sean Carroll, pg 17. "The Making Of The Fittest: DNA And The Ultimate Forensic Record of Evolution". 2006. From the author also of "Endless Forms Most Beautiful: The New Science of Evo Devo".


Three more recent scientific discoveries in the fields of genetics appear to many to be the strongest evidence yet for evolution, including macroevolution.  Some scientists have even stated that the fossil record is now no longer needed to support evolution due to discoveries like these, but fossils are now rather frosting on the 'cake' of evolutionary evidence.  These three discoveries are endogenous retroviruses (ERVs),  human chromosome 2 fusion, and pseudogenes.


1. Endogenous Retroviruses


There are viruses that contain RNA instead of DNA.  After absorbing itself into a host cell during infection, it must first make a copy of DNA from its RNA (transcribe it) before it can integrate its viral genome into the host DNA.  Thus, it first must reverse transcribe and therefore these viruses are known as retroviruses.  It does this first step by using a viral enzyme called reverse transcriptase that was part of the viron particle.  Reverse transcriptase is not very efficient and often makes mistakes, producing random mutations.  Once integrated into the host DNA and genome the viral genome is now called a provirus.  The cell then divides and the provirus is replicated along with the host genome.  Later, certain conditions can trigger provirus activation and billions of new viral particles are assembled by the host cell and eventually released through budding.  These new virons float off and infect new cells; the original host cell dies.


HIV Life Cycle: Example of a Retrovirus

























However, the retrovirus faces a problem. In order for the provirus to be activated by the host cell, there needs to be an adjacent section of DNA called a promoter present. If there was only one set of promoters, the first transcribed viral genome would have no subsequent promoters since the host enzyme that is used does not copy the promoter.  The retrovirus solves this problem by making multiple copies of its promoters during the time reverse transcriptase is operating.  Due to certain biochemical constraints, these sections are all nearly identical at the time of insertion and are called Long Terminal Repeats or LTRs (importance to come). When the viral genome is inserted into the host DNA, a short section of the host DNA is duplicated in order to make the two broken ends fit.  Target site duplication is a way scientists can tell when there has been an insertion event.   If an infected host cell happens to be a sex cell (sperm or egg), the provirus can be passed down through generations of offspring.  Cells do not have a way to remove the provirus without deleting host DNA or leaving LTRs behind,  so they tend to remain.  Additionally, ERVs tend to accumulate mutations at the same rate as large areas of the host genome that do not code for genes.  Over time, the mutations become fixed in the host's gene population pool and eventually enough mutations build up to make the ERV nonresponsive to activation.  It's now basically a fossil viral genome and endogenous since it is found as a permanent part of the host genome.


If you find two individuals of any species with the same ERV at the same loci (loction on a chromosome), you know that they shared a common ancestor. Why?  First, because the integration points tend to be highly random and second, these ERVs can have shared identical mutations; it would be impossible for two individuals to have the same ERVs at the same location within their genome with similar random mutations unless they shared a common ancestor.  Thus, this is ancient evidence that we, for example, share ancestors and origins with chimps and monkeys.  This is powerful and spectacular macroevolution evidence right from our own DNA when compared to other primates.  Let's now turn to the human genome.  If evolution is true, we should find supporting evidence by comparing ERVs from different species and/or individuals.


1. Shared ERVs.  About 8% of our DNA consists of ERVs (!), so there is much available material to use in comparisons.  We share some of our ERVs with chimps, great apes, old world monkeys,  new world monkeys and even Prosimians.  And these ERVs are not grouped randomly between species, but can be arranged in subsets or hierarchies. These subsets can be nested into larger and larger groups that align with evolutionary relationships derived from other fields of study such as the fossil record and demonstrate we share a common ancestry with other species of primates.


2. Shared LTR mutations.  As mutations build up in the LTRs, the variability in the ERVs increases.  ERVs between species at the same locus that have more variability in their mutations correlate to older insertions. Evolution predicts that we would find higher ratios of discontinuity between LTR sections when comparing species with wider taxonomic separation and that is exactly what we observe.


3. Shared ERV mutations. An examination of shared ERVs between species demonstrates identical mutations in some.  These also can be arranged in a nested hierarchy. In other words,  some are shared by all, but some only by closer related species.


4. Different nested hierarchies match. The nested hierarchies from the ERV distribution match the nested hierarchy of the LTR discontinuity ratios,  despite the fact that the two rely on different mechanisms (integrase activity vs. the DNA replication complex). These also match the fossil record.





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