One of the most brilliant evolutionary biologists of the present day, Richard Sternberg, PhD PhD was ousted and permanently blacklisted by the National Institutes of Health and the Smithsonian Museum for his ID sympathies.
Sternberg is neither a Creationist nor Darwinist but classifies himself as a Process Structuralist which means he is not much involved in the ultimate questions of how things came to be, he just appreciates the amazing patterns of similarity and diversity in biology.
He was labelled by some of his former supporters as an intellectual terrorist after he used his position as editor of a journal to publish an ID-friendly article by Stephen Meyer in 2004. He paid dearly for that decision, and his subsequent dismissal from the NIH and Smithsonian precipitated special investigations by members of Congress and the White House a decade ago. Unfortunately, nothing of consequence was done for Sternberg and he was destroyed professionally and personally.
Despite his circumstances, he continued to publish excellent essays such as the one that highlights the non-random patterns of SINES (presumed by some to be junkDNA) which are present in mice and rats (link below).
To understand his essay, I will describe the essentials of his essay with a parable. Suppose we had two mostly identical stories published. The stories are identical except for the fact that in one version of the story the name of the main character is “Mary” and in the other version, the name of the main character is “Caroline”. Even if the two versions of the stories were generated from the same template, the changes in the two descendant copies could not have been random.
So even if we assume some sort of common descent of the two versions of the story from some ancestral copy, the differences in the versions could not be the result of random copying errors, but very deliberate and methodical changes in the duplication process that created the two versions. This peculiar phenomenon plays out approximately in the genomes of mice and rats, and I call it the Sternberg-Collins paradox in honor of Sternberg who brought the paradox into prominence and Francis Collins who was among the first to comment on the anomaly.
Assume for the sake of argument rats and mice came from a common ancestor. Are there differences which are non-random and thus evidence for non-random mutation? Sternberg effectively answers, “yes”.
The mouse and rat genomes look very similar, but there are sequences that repeat over and over again in each of their respective genomes and mostly in the same corresponding locations. If these sequences were identical in both lineages, there would not be much of an issue, but they are different even though they are in the same general corresponding locations.
Let me call one set of these repeating sequences in the mouse genome “Mary” and the corresponding sequence in the rat genome “Caroline”. The name “Mary” appears in numerous places in the mouse genome, and in the corresponding places where “Mary” appears in the mouse genome, “Caroline” appears in the rat genome.
Of course this was a figurative way of describing what is going on. “Mary” is in reality the B1/B2/B4 set of SINE retro elements in mice, and “Caroline” is in reality the ID SINE retro elements in the mouse. But don’t get hung up on the fancy language, the basic problem of non-random changes from a supposed common ancestor is brutally evident. A graph that shows the non-random changes is here and explained in Sternberg’s essay:
Sternberg’s point is that if mutational events happened, it was non-random, since to suppose it was random is an absurdity in the extreme. It cannot be the result of random DNA copying errors, but some non-random copying mechanism if common descent were true.
Is the non-random pattern the result of natural selection? Sternberg doesn’t address that question. But if the non-random SINE pattern is the result of selection, then this would mean the SINES aren’t junkDNA.
But if natural selection is assumed as the mechanism, there would be issues of the evolvabilty of so many nucleotides simultaneously. We’re talking maybe 300,000 SINE insertions in each lineage! For mice, the B1 sine is about 150bp and homologous to the 300bp primate Alu. The B2 SINE is 190bp. I could not find the size of the rat ID SINE nor the mouse B4 SINE, but I presume they are within the range of most other SINES (75-400 bp).
The source article in Nature which Sternberg referenced and had a buzzillion co-authors can be found here:
Genome sequence of the Brown Norway rat yields insights into mammalian evolution
That article points out:
Despite the different fates of SINE families, the number of SINEs inserted after speciation in each lineage is remarkably similar: approx300,000 copies.
Sternberg highlights the issue of having 300,000 non-random insertions happening in parallel in the two lineages after they split. He lays out the paradox which is the focus of this OP here:
Beginning to Decipher the SINE Signal
FWIW, I suspect there are probably similar issues with the Alu elements that appear in primates. Certainly this would be an issue if the mouse B1 (homologous to primate Alu) is in homologous locations in the primate genome. If that is the case, the Sternberg-Collins paradox is in play as well for primates. Perhaps one day we’ll know for sure if this is the case.