Primate evolution in the fast laneWow!! What is it then??
The pace of evolution is typically measured in millions of years, as random, individual mutations accumulate over generations, but researchers at Cornell and Bar-Ilan Universities have uncovered a new mechanism for mutation in primates that is rapid, coordinated, and aggressive. The discovery raises questions about the accuracy of using the more typical mutation process as an estimate to date when two species diverged, as well as the extent to which this and related enzymes played a role in primate evolution.
Alon Keinan, associate professor of Biological Statistics and Computational Biology at Cornell, and Erez Levanon, co-senior author and an associate professor with the Mina and Everard Goodman Faculty of Life Sciences at Bar-Ilan University in Israel, describe the novel, and rare, process triggered by a member of the APOBEC family of virus-fighting enzymes in the journal Genome Research. As primates evolved--including chimpanzees, Neanderthals, and modern humans--the number of types of viruses tailored for targeting primates multiplied. APOBECs in our cells mount a vigorous defense, bombarding the viral genome with clusters of mutations to render them unable to continue an infection. However, having such a mutation-based defense is risky for cells, since "friendly fire" could wreak havoc on our genome as well. Indeed, the enzymes have been shown to cause mutations in the tumor cells of breast and other cancers.So the "friendly fire" which attacks the single strand DNA of a virus with mutations which render it inoperable... will cause beneficial mutations, producing primates?
The discovery is particularly significant because the enzyme has a tendency to alter regions of the genome that code for proteins as well as the areas responsible for their regulation. It's a vestige of their primary function in viral defense: Many viruses are composed of single stranded DNA or RNA, and DNA being actively used as a template for proteins is temporarily single stranded and unwound from the double helix. To the enzyme, they look the same.So what, exactly, do we have here?
The researchers looked for the signature of past mutations in humans and our closest hominid relatives, focusing on one of the enzymes in the APOBEC family, APOBEC3, since it has expanded into several subtypes during primate evolution, each with unique mutational signatures.
They knew that the enzyme recognizes a specific motif in the DNA and it targets only one of the DNA bases for mutation. Another telltale sign: multiple mutations occurring close together. Using conservative criteria, they identified thousands of such instances unique to primate genomes and, as negative control, did not identify any in other vertebrates such as mice that lack many of the APOBEC3 genes.
"What is appealing is that it's an accelerated evolutionary mechanism that could generate a large change in a gene in a single generation," said Levanon. "It's like playing the lottery--it could not have an impact, or it could have a major one."
"These events potentially mutate dozens of DNA bases in a small region less than the size of a gene. It is reasonable to think that most of these mega-mutations will be deleterious and will disappear in evolutionary time, but we do see a large number that survived," added Keinan. "Importantly, those that survived are overrepresented in functionally important parts of the genome, which suggests that some of these mutations have been maintained by natural selection because they conferred an advantage."
1. An enzyme which is part of the viral defense system can attack the Host DNA, leaving a mutated DNA behind.
2. This occurs only on single strand DNA, meaning that APOBEC3 attacked genetic DNA during reproduction, when it is split into single strand.
3.They looked at "mutations" (apparently a mutation is defined as "looking like the "signature" left by the attack enzyme, AND being different from mouse DNA"). They found lots of those, with the "mark" of that virus-killer enzyme.
Now, do they know that these are mutations, or are they merely defined as mutations because they are not the same as mouse DNA? It should be obvious that mouse construction is not the same as ape or human construction. So because evolution by mutation is presupposed as a First Principle, then it must be an evolutionary trait, rather than a mere difference between two similar but not identical things. Differences would not be called beneficial mutations without first presupposing that evolution is a First Principle.
Do they know that the "mutations" which are presumed to be carried over and propagated throughout a population are actually mutations, or could they just "look like" mutations, because mutations are what they were looking for?
If these actually were mutations and are really beneficial, as in creating something that mice don't have, then what is it? Or are they negative, deleterious mutations as in, say, removing the tail or body fur? Or more likely, are they even active at all, since random changes don't add information, they either subtract information or in rare cases are neutral. And even more likely yet, they have no idea whatsoever about what these "mutations" do, if anything, or even if they really are mutations.
What is the likelihood of APOBEC3 attacking a temporarily unwound host DNA in a sperm or egg cell, and coincidentally creating beneficial features which differentiate higher apes and humans from mice? The authors even admit that it's like winning the lottery (it's probably far, far less likely than that allusion), and they admit that most such "mutations" would be deleterious and selected for destruction rather than propagation throughout a population. And that is especially the case if APOBEC3 mutates "dozens of DNA bases in a small region less than the size of a gene". That many "mutations" would be exponentially unlikely to produce valid and valuable information - especially while maintaining prior functionality. In fact, if there are "dozens of changes" from the mouse genome, and they are functional, then the actual overwhelming likelihood is that they were not mutations at all. Instruction books don't get better by making lots of random changes to the instruction set in the original book.
Further yet, if this is an evolutionary process then why don't viruses sprout new features when they are attacked? In fact, why does such a process exist at all? What are the chances that an APOBEC family of "attack by mutation" enzymes came to exist... by virtue of some sort of mutation chain or cluster which was sequestered away until it became a complete and useful enzyme, stored in DNA somewhere? This question becomes acutely focused on evolution now that we know that all - ALL - the information in DNA is used, and even double coded; mutating any of it necessarily destroys functionality.
Well, the standard response to that issue (actually all issues) is "Deep Time", of course. Given enough depth of time, minerals overcome entropy to become living cells, and single cells mutate into all the phyla, which in turn mutate into hordes of creatures most of which die off while others increase in complexity until some of them become intelligent enough to create Creation Stories as "science", without the need for actual empirical evidence.
And why would the segment which has been accidentally mutated by "friendly fire" not be considered a loss of useful information? Would such mutations not be expected to pervert or destroy existing necessary functionality, every time such a mutation occurred? Or is the expectation that such mutations served two functions: to a) maintain prior functionality while b) simultaneously creating new, selectable advantageous features resulting in primates? The chances against that are staggeringly and vanishingly small, to the point of absolute absurdity.
Returning to the claims in this paper, what they actually know is that they found multiple cases of DNA segments, even within a gene, which resemble the effects which are caused by APOBEC3 viral killer mutations.
And here's what they do not actually know: these similarities are presumed but not known to be caused by APOBEC enzymes, and thus presumed but not known to be useful for rapid mutation resulting in beneficial characteristics, as the assumption is applied to the emergence of primates. This is presumed but not known to be the case, even thugh such mutations would generally be thought to be destructive of necessary information and therefore would necessarily be deleterious, due to eradicating information for making and/or expressing the proteins which were already being used prior to the supposed mutation.
Since they don't even know what the "mutations" do, if anything, much less how they actually got there, they are released from any boundary conditions on what they can speculate. And the true believers are not likely to question whether the speculation actually makes sense, especially in terms of overall probabilities and the absurdities determined by Reductio Ad Absurdum.
Overall, this paper fails to produce new, objective knowledge regarding actual evolution.