It is simply a matter of time before the Darwinists (I know they prefer “evolutionary biologists,” but evolution is not evolution without “Origin of Species”) will have to give up.
Every day in labs around the world, more and more function is being found for “junk” DNA. This is a two-fold problem for the Darwinists.
The first problem is that this is NOT what they predicted, even though, quite cavalierly, they say then never said any such thing. But, of course, we know better.
Second, there’s the problem of “de novo” genes, and the solution for this is to look to so-called “junk” DNA as a potential template for these ‘new’ genes. If “junk” DNA is ‘neutral,’ then no problem; but if it has a function, then the nursery from which they can harvest “de novo” genes from within the genome lessens. As I say, it’s a matter of time.
From Phys.Org we have a snippet from a news summary:
In the first study to run a genome-wide analysis of Short Tandem Repeats (STRs) in gene expression, a large team of computational geneticists led by investigators from Columbia Engineering and the New York Genome Center have shown that STRs, thought to be just neutral, or “junk,” actually play an important role in regulating gene expression. The work, which uncovers a new class of genetic variants that modulate gene expression, is published on Nature Genetics’s Advance Online Publication website on December 7.
Erlich’s study looked at Short Tandem Repeats (STRs), variants that create what look like typos: stutter vs. stututututututter. Most researchers, assuming that STRs were neutral, dismissed them as not important. In addition, these variants are extremely hard to study. “They look so different to analysis algorithms,” Erlich notes, “that they just usually classify them as noise and skip these positions.”
And, revealing a mechanism I have long suspected could be the true purpose, or function, of these repeated elements, they say:
Erlich used a multitude of statistical genetic and integrative genomics analyses to reveal that STRs have a function: they act like springs or knobs that can expand and contract, and fine-tune the nearby gene expression. Different lengths correspond to different tensions of the spring and can control gene expression and disease traits.