As Luck Would Have itnew research suggests yet another adaptive mutation mechanism.
The DNA double helix consists of two long strands wrapped around each other. Protein-coding genes can be on either strand, but one strand is more prone to mutations. This is because on that strand the DNA copying (replication) machine and the gene copying (transcription) machine move in opposing directions, and so head-on confrontations can occur. The new paper makes good arguments that these confrontations result in a higher mutation rate for genes on that strand.
Yet there are many genes on the “head-on” DNA strand. Why would that be? The new paper provides multiple evidences that not only these genes have incurred more mutations than normal, but that those mutations have often been helpful. That is, those mutations often have been adaptive.
So the paper hypothesizes that those genes are in the “head-on” orientation for good reason. They were genes that needed more mutations. The authors hypothesize a “replication–transcription conflict-mediated mutagenesis” strategy where genes that the organism particularly needs to modify are in the “head-on” DNA orientation.
This new hypothesis is not without its questions. For instance, while the “head-on” genes seem to reveal elevated levels of adaptive mutations, they do not show higher levels of mutations that do nothing to the protein’s amino acid sequence (the so-called synonymous mutations). Synonymous mutations are normally taken to reflect the underlying mutation rate. So if the mutation rate is higher due to a “head-on” orientation, then one would expect the synonymous mutation rate to be higher. That is standard evolutionary reasoning.
Another question is how and why do the genes switch from one DNA strand to the other, in the first place? In other words, this new strategy requires that genes switch from one strand to the other at some regular frequency. Whatever the mechanism, it must perform this switching at a rate that is not too low (or else very few genes would ever switch and evolutionary experimentation would be impossible) and not too high (or else the distribution between strands would be more random).
Finally there is, once again, the issue of serendipity. Under this new hypothesis evolution must have created a gene strand switching mechanism with an appropriate frequency. Such a mechanism would not provide any fitness improvement immediately. Instead the mechanism would set about switching, at random, genes from the strand they are on to the opposing strand.
And any such switches would also fail to provide fitness improvement immediately. But over time, some switches would help when certain genes undergo higher mutation rates. All of this means that evolution would have to create a sophisticated mechanism that only much later would provide benefit.
A typical explanation is that the new mechanism was simply a result of the combining of existing parts that were “lying around.” But this does nothing to reduce the serendipity involved. The bottom line here is that the new evidence forces evolutionary theory to take on even more complexity and serendipity. Evolution creates evolution.