Sexual selection: who bastardized Darwin’s theory?
February 13, 2013 | James Kohl
Charles Darwin (1809 – 1882) Charles Darwin: gentleman naturalist A biographical sketch by John van Wyhe
Excerpt: “Darwin also identified another means by which some individuals would have descendants and others would not. He later called this sexual selection. This theory explained why the male sex in many species produce colourful displays or specialised body parts to attract females or to compete against other males.”
My comment: Since 1996, descent with modification has included the molecular mechanisms of alternative splicings that enable the evolution of nutrient-dependent sex differences, which are maintained in species via pheromone-controlled reproduction. Adaptive evolution is nutrient-dependent from the bottom up and it is pheromone-controlled from the top down.
How was mutations theory paired with Darwin’s theory? Does anyone believe that mutations caused the evolution of nutrient-dependent sex differences in pheromone production that enable sexual selection via the metabolism of the nutrients to species-specific pheromones in species from microbes to man? Is there a model for that?
Natural selection is for food. Sexual selection is for nutrient-dependent pheromone production. Adaptive evolution is nutrient-dependent and pheromone-controlled. Who bastardized Darwin’s theory?
Molecular epigenetics: from Diamond, Binstock, and Kohl (1996)
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.