Failed attempts to support the role of randomness in evolution

Randomness and gene expression and evolution?

Robinson R (2013) Bursting with Randomness: A Simple Model for Stochastic Control of Gene Expression. PLoS Biol 11(8): e1001622. Excerpt: “The model the authors developed provides a structural basis for transcriptional bursting consistent with a large body of data. While other models might also explain that data, none do so as simply and with as few “working parts” as theirs—generally a sign that a model is pointing in the right direction.”

Brown CR, Mao C, Falkovskaia E, Jurica MS, Boeger H (2013) Linking Stochastic Fluctuations in Chromatin Structure and Gene Expression. Excerpt: “The number of mRNA and protein molecules expressed from a single gene molecule fluctuates over time. These fluctuations have been attributed, in part, to the random transitioning of promoters between transcriptionally active and inactive states, causing transcription to occur in bursts. However, the molecular basis of transcriptional bursting remains poorly understood.”

My censured comment: The molecular basis of nutrient-dependent pheromone-controlled transcriptional bursting has been exquisitely detailed. Jay R. Feireman posted these two examples (above) to the ISHE human ethology group, but would not allow my response. That exemplifies a back-handed attempt to support the role of randomness in evolution compared to the obvious role of nutrient uptake and the metabolism of pheromones to species-specific pheromones that control reproduction. Controlled reproduction eliminates the role of randomness in adaptive evolution. Since a model organism for stochastic control of gene expression is yeast, and the yeast model is featured in both of the links above, here are links from me that clarify nutrient-dependent pheromone-controlled reproduction in yeasts, while extending the concept to humans via conserved molecular mechanisms.

Gene duplication as a mechanism of genomic adaptation to a changing environment [Open access]

Excerpt: A clear example of a gene duplication conferring an adaptive response to nutrient limitation is that of the yeast hexose transporter. Under growth conditions with low glucose, the appearance of a new hybrid copy from two closely related paralogues, HXT6 and HXT7, increases the level of expression of the hexose transporter and, crucially, the rate of glucose transport into the cell [41].

Excerpt: One of the main duplicated gene families are the olfactory receptor proteins [18,117–119] so perhaps their duplication may lead to an increase in sensitivity to a particular odour may be adaptive under certain conditions.

We attempted to clarify the fact that chromatin structure and gene expression link yeasts to mammals via nutrient-dependent pheromone-controlled reproduction in our 1996 Hormones and Behavior review, which included a section on molecular epigenetics. From Fertilization to Adult Sexual Behavior.

Excerpt: “Yet another kind of epigenetic imprinting occurs in species as diverse as yeast, Drosophila, mice, and humans and is based upon small DNA-binding proteins called “chromo domain” proteins, e.g., polycomb. These proteins affect chromatin structure, often in telomeric regions, and thereby affect transcription and silencing of various genes (Saunders, Chue, Goebl, Craig, Clark, Powers, Eissenberg, Elgin, Rothfield, and Earnshaw, 1993; Singh, Miller, Pearce, Kothary, Burton, Paro, James, and Gaunt, 1991; Trofatter, Long, Murrell, Stotler, Gusella, and Buckler, 1995). 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 others continue to ignore the fact that I addressed these molecular mechanisms with co-authors in 1996, and to also infer that evolution is “Bursting with randomness” or that stochastic gene expression is not nutrient-dependent and pheromone-controlled exemplifies how they manipulate information dissemination rather than allow accurate representations of established biological facts.