The central dogma of evolutionary biology: Random mutations

A new gene-expression mechanism is a minor thing of major importance August 21st, 2013 in Biology / Cell & Microbiology

Excerpt: “… a single inefficiently spliced minor intron can hold up expression – mRNA and protein production – for an entire gene. ”

I’m posting this link to the elife article so that someone who reads it can tell me how random mutations might be involved in evolution. Could, for example, a random mutation hold up expression for an entire gene, or cause expression of another?

Minor introns are embedded molecular switches regulated by highly unstable U6atac snRNA

Excerpt:  “The central dogma of biology states that genetic material, DNA, is transcribed into RNA, which is then translated into proteins. However, the genes of many organisms have stretches of non-coding DNA that interrupt the sequences that code for protein.”

Here, we have a  small RNA (not DNA) that turns a gene-splicing machine into a switch that controls the expression of hundreds of human genes. The role of the small RNA in changing the microRNA/messenger RNA balance seems to be clear, as it is most likely to do that so that protein biosynthesis and degradation is ‘matched’ to the sensory environment that requires the match. But the requirement for the match eliminates the central dogma of evolutionary biology that’s been used to tout mutation-driven evolution.  Thus, the article is of major importance to those who would like to continue to cling to mutations theory. (They will need help refuting evidence.)

Someone like David Leake may note that “The importance of the minor spliceosome has been recently underscored by reports that mutations in U4atac cause microcephalic osteodysplastic primordial dwarfism type I (MOPD I) or Taybi-Linder syndrome (TALS) (Abdel-Salam et al., 2011; Edery et al., 2011; He et al., 2011).” Someone may even claim that supports natural selection for mutations — until they realize it must result in natural selection for dwarfism. Adaptive evolution, for comparison, is nutrient-dependent and pheromone-controlled.

Excerpt:  “Fine-tuning the level of the catalytic snRNP, U6atac, allows for a circuit design based on the capacity to completely shut off or rapidly up-regulate the production of the full-length mRNAs from a pool of pre-mRNAs in which all the other major introns have been spliced, without having to affect their transcription (Figure 7). Indeed, as our RNA-seq show, a single minor intron is sufficient to regulate the expression of an entire pre-mRNA. The conservation of this design principle over >500 million years (Burge et al., 1998; Shukla and Padgett, 1999; Russell et al., 2006) demonstrates the effectiveness of this gene regulation mechanism.”

Would someone please offer an explanation for their belief that random mutations could be involved in adaptive evolution over >500 million years of effective gene regulation? Is there a model for that? In my mammalian model, “Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to sexual differentiation in at least two species, Drosophila melanogaster and Caenorhabditis elegans (Adler and Hajduk, 1994; de Bono, Zarkower, and Hodgkin, 1995; Ge, Zuo, and Manley, 1991; Green, 1991; Parkhurst and Meneely, 1994; Wilkins, 1995; Wolfner, 1988). That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes.”

That doesn’t mean the same sex differences are conserved during over >500 million years of effective gene regulation. It simply means that the molecular mechanisms of effective gene regulation in adaptive evolution have been conserved.