Drosophila’s New Genes
An analysis of the transcriptomes of several fruit fly strains reveals dozens of possible de novo genes in each.
By Jef Akst | January 23, 2014
Excerpt 1: “There has been a long tradition in biology to think that a gene can only arise due to duplication and diversions from another gene, and this is therefore a completely new story.”
Excerpt 2: “It shows the power of generating from nothing, so to speak.”
My comment: “The de novo creation of genes has previously been reported to be the “holy grail” of evolutionary biology. If that is true, what’s reported here exemplifies the fact that the “holy grail” involves only the direct olfactory/pheromonal link from the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man.
See, for example, our 1996 Hormones and Behavior review article: From Fertilization to Adult Sexual Behavior (e.g., the section on molecular epigenetics where TB wrote): “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…”
The alternative splicings are obviously nutrient-dependent and they lead to 1) de novo gene creation and 2) chromosomal rearrangements, which are exemplified in sex diffferences at the advent of sexual differentiation in the cell types of yeasts that sexually reproduce. The physiology of reproduction is controlled by the metabolism of nutrients to pheromones in species from microbes to man. That means de novo creation of genes probably occurs via conserved molecular mechanisms in all species (see: Organizational and activational effects of hormones on insect behavior).
Alternatively, mutation-driven evolution can be substituted for the nutrient-dependent pheromone-controlled ecological adaptations that enable the de novo creation of genes and species divergence. However, it has become apparent that “… natural selection is an evolutionary process initiated by mutation. It does not have any creative power…” (p. 196: Mutation-Driven Evolution). Therefore, theorists must explain how natural selection for mutations occurs so that their theory can be compared to a model of ecological variation, natural selection of food, and de novo gene creation.
The model incorporates what is required for the Creation of new genes that enable organismal complexity via ecological, social, neurogenic, and socio-cognitive niche construction. What’s required is food and nutrient-dependent pheromone-controlled reproduction. See for example: Nutrient-dependent/pheromone-controlled adaptive evolution: a model
James V. Kohl detailedl how quantized energy-dependent microRNA biogenesis links the pheromone-controlled physiology of reproduction to biophysically constrained viral latency and healthy longevity. Links from what organisms eat to the enzyme-dependent metabolism of food also link metabolic networks to microRNA-mediated genetic networks in the context of RNA interference. Drug therapies alter RNA interference by altering cell type differentiation in all cells of all individuals of all species. For comparison, during the past 26 years, Kohl has detailed how the chemistry of protein folding is biophysically constrained at every level of biological organization by conserved molecular mechanisms.