Let’s face it: humans are kinda narcissistic. For those of us who are evolutionarily-minded, as such we have a tendency to envision ourselves as lying at the pinnacle of eukaryotic development– in spite of our better attempts at reminding ourselves that “evolution has no aim.” But after all, with our brilliant brains, why shouldn’t we consider some aspects of evolution as “progressive”? For instance, we as humans have changed so much structurally since the time of our last common ancestor with the chimpanzees, meanwhile chimps bear much more resemblance to the ancient apes.
And when we look at overall genome size, even though there are notable exceptions such as the onion or the gray short-tailed South American opossum, “higher order” organisms tend to have larger genome sizes. So there is an air of progressiveness in evolutionary development.
Yet in spite of appearances, we forget that genetic evolution doesn’t stand still across species. And since we typically haven’t got access to ancient genomes but only to modern ones, it’s all too easy to assume that we have evolved while lesser organisms, such as mollusks for instance, have stood largely stock still. True, morphologically (structurally), a clam may be little removed from its ancestor of hundreds of millions of years ago, while we have changed remarkably since our last cephalopod relative.
Genetically, however, more lurks beneath the surface than meets the eye. Little would you know, but most eukaryotic genomes have evolved to become more streamlined than those of their ancient relatives. When we take a look at the numbers of introns, for instance, which are the segments of non-coding DNA in genes that separates the protein-coding exons, modern eukaryotes typically have far fewer introns than has been estimated for their last common ancestor. This means that animals, plants, and fungi– we have all tended to lose introns over time . And this has occurred after each of these kingdoms diverged from one another, making this probably one of the widest-spread cases of convergent evolution.
The mechanisms of these losses are uncertain, although I would hazard to say it has to do with genetic recombination– otherwise known as copy number variations (CNV) in modern day pathological parlance. The occurrence rates of CNV deletions outweigh the number of duplications by about 2:1, primarily because the mechanisms for creating deletions are comparatively simpler and therefore much more likely to occur than that of duplications. This makes recombinatory deletions a leading probable cause of genetic streamlining.
Interestingly, those species who have tended to “break even” in terms of intron loss and gain over the millenia include species such as ourselves and the plant, Arabidopsis, suggesting that there is strong positive selection for certain introns in our genomes, most likely a reflection of strongly conserved non-coding regulatory sequences.
Where do genetic changes come from? It’s a question seldom asked. Michael Rutter is one who asked this question as it occurs in de novo genetic changes in ASD.
Do you have an article where Rutter ponders that Q, Robert? I’m more familiar with his older work.
It was at a conference at Duke University on Gene Environment interplay. A 30 minute video and you will find it here. Excellent talk and will worth the 20 minutes: