PaV asks us to draw attention to this new paper on transposons, transposons:
Until recently, little was known about how transposable elements contribute to gene regulation. These are little pieces of DNA that can replicate themselves and spread out in the genome. Although they make up nearly half of the human genome, these were often ignored and commonly thought of as “useless junk,” with a minimal role, if any at all, in the activity of a cell. A new study by Adam Diehl, Ningxin Ouyang, and Alan Boyle, University of Michigan Medical School and members of the U-M Center for RNA Biomedicine, shows that transposable elements play an important role in regulating genetic expression with implications to advance the understanding of genetic evolution.
Transposable elements move around the cell, and, unlike previously thought, the authors of this paper found that when they go to different sites, transposable elements sometimes change the way DNA strands interact in 3-D space, and therefore the structure of the 3-D genome. It appears a third of the 3-D contacts in the genome actually originate from transposable elements leading to an outsized contribution by these regions to looping variation and demonstrating their very significant role in genetic expression and evolution.
University of Michigan, “ Transposable elements play an important role in genetic expression and evolution” at Phys.org
SoPaV notes, it’s this “useless junk,” the same “junk” that ID theorist said the “blueprint” is to be found, which actually drives speciation.
He draws our attention to the end of the Discussion section in the Nature Communications paper (open access):
“We postulate that TE-induced population-level looping variability in the MRCA [most recent common ancestor] of human and mouse may have conferred adaptive advantages that allowed certain individuals to flourish in the face of changing selective pressures. This, in turn, may have led to divergence between subpopulations as they adapted to distinct evolutionary niches, eventually leading to speciation. This work advances our understanding of the relationship between TEs and their host genomes, raising important questions about the interplay between the role of CTCF in TE biology, the necessity of CTCF variability in host chromatin dynamics, the evolutionary forces driving looping variability, and their effects on adaptation to a changing environment.”
Zero to hero in one easy Darwinian rewrite? Naw. Not so fast. Not any more. Few questions first.
For one, why was it so easy to assume they were useless junk? And now suddenly they’re Mr. Fixit?