Why would a system exist that reduces the vigor of potential mates prior to mating? Addressing this question could provide insights into mechanisms and evolution of sexual conflict and reveal sensory inputs that regulate aging.
An unknown signal accelerates larval development, specifically the onset of puberty
“There is a fine balance between reproduction and body maintenance, and this balance can be tipped by the male. We now are starting to tease apart this complexity.”
Body maintenance is a nutrient energy-dependent ecological adaptation. Energy theft is linked to mutations, which cannot be linked to biophysically constrained RNA-mediated biodiversity via the energy-dependent function of the innate immune system. That fact requires theorists to express their links to cell type differentiation in terms that attribute all extant biodiversity to unknown signals and/or pheromones.
Theorists have no model that links ecological variation to accurate representations of energy-dependent biologically-based cause and effect. Now, an unknown signal must be included in their theories at a time when all serious scientists have detailed all the links from energy-dependent changes in angstroms to ecosystems in all living genera.
This atoms to ecosystems model of ecological adaptations links nutrient-dependent epigenetic effects on base pairs and amino acid substitutions to pheromone-controlled changes in the microRNA / messenger RNA balance and chromosomal rearrangements. The nutrient-dependent pheromone-controlled changes are required for the thermodynamic regulation of intracellular signaling, which enables biophysically constrained nutrient-dependent protein folding; experience-dependent receptor-mediated behaviors, and organism-level thermoregulation in ever-changing ecological niches and social niches. Nutrient-dependent pheromone-controlled ecological, social, neurogenic and socio-cognitive niche construction are manifested in increasing organismal complexity in species from microbes to man.
Re: An unknown signal… See: Feedback loops link odor and pheromone signaling with reproduction
The “unknown signal” must be a nutrient energy-dependent food odor or a pheromone. No other signal links the epigenetic landscape from the innate immune system to the RNA-mediated physical landscape of supercoiled DNA in species from microbes to humans.
Evolutionary Rewiring (bacteria)
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.
“Tight DNA packaging” and “tightly coiled DNA” are terms used to obfuscate the facts about supercoiled DNA that have already linked viral latency to all pathology.
Supercoiled DNA protects the organized genomes of all living genera from virus-driven entropy. That fact has been the focus of my efforts.
Who else seems to be following the literature on RNA-mediated cell type differentiation?
Between you and your neighbor, there’s only about 0.1 percent difference between your two sets of DNA. Even more, scientists think that this small difference affects the way many parts of the human body are designed: eye color, hip shape, and your chance of becoming sick.
“Variation is not only important for how genes and proteins function, but it can also occur in the noncoding, repetitive portions of the genome. “What we found in this study is probably the tip of the iceberg. There could be all sorts of functional consequences to having variation within the complex, repetitive portion of the genome that we don’t know about yet.”
All serious scientists already know that heterochromatin function is nutrient energy-dependent and transgenerationally inherited via epigenetic effects of sensory input that alters the microRNA/messenger balance. Epigenetically altered morphological and behavioral phenotypes are linked from the innate immune system to heterochromatin function because it top-down causation did not link the immune system from metabolic networks to genetic networks in all organisms, the biodiversity of life on Earth would not exist.
A defining feature of heterochromatin is methylation of Lys9 of histone H3 (H3K9me), a binding site for heterochromatin protein 1 (HP1). Although H3K9 methyltransferases and HP1 are necessary for proper heterochromatin structure, the specific contribution of H3K9 to heterochromatin function and animal development is unknown. Using our recently developed platform to engineer histone genes in Drosophila, we generated H3K9R mutant flies, separating the functions of H3K9 and nonhistone substrates of H3K9 methyltransferases. Nucleosome occupancy and HP1a binding at pericentromeric heterochromatin are markedly decreased in H3K9R mutants. Despite these changes in chromosome architecture, a small percentage of H3K9R mutants complete development. Consistent with this result, expression of most protein-coding genes, including those within heterochromatin, is similar between H3K9R and controls. In contrast, H3K9R mutants exhibit increased open chromatin and transcription from piRNA clusters and transposons, resulting in transposon mobilization. Hence, transposon silencing is a major developmental function of H3K9.