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.

 

About James V. Kohl 1308 Articles
James Vaughn Kohl was the first to accurately conceptualize human pheromones, and began presenting his findings to the scientific community in 1992. He continues to present to, and publish for, diverse scientific and lay audiences, while constantly monitoring the scientific presses for new information that is relevant to the development of his initial and ongoing conceptualization of human pheromones. Recently, Kohl integrated scientific evidence that pinpoints the evolved neurophysiological mechanism that links olfactory/pheromonal input to genes in hormone-secreting cells of tissue in a specific area of the brain that is primarily involved in the sensory integration of olfactory and visual input, and in the development of human sexual preferences. His award-winning 2007 article/book chapter on multisensory integration: The Mind’s Eyes: Human pheromones, neuroscience, and male sexual preferences followed an award winning 2001 publication: Human pheromones: integrating neuroendocrinology and ethology, which was coauthored by disinguished researchers from Vienna. Rarely do researchers win awards in multiple disciplines, but Kohl’s 2001 award was for neuroscience, and his 2007 “Reiss Theory” award was for social science. Kohl has worked as a medical laboratory scientist since 1974, and he has devoted more than twenty-five years to researching the relationship between the sense of smell and the development of human sexual preferences. Unlike many researchers who work with non-human subjects, medical laboratory scientists use the latest technology from many scientific disciplines to perform a variety of specialized diagnostic medical testing on people. James V. Kohl is certified with: * American Society for Clinical Pathology * American Medical Technologists James V. Kohl is a member of: * Society for Neuroscience * Society for Behavioral Neuroendocrinology * Association for Chemoreception Sciences * Society for the Scientific Study of Sexuality * International Society for Human Ethology * American Society for Clinical Laboratory Science * Mensa, the international high IQ society