…will need to disentangle whether sex genetic heterogeneity may arise as a consequence of interactions with genetic loci located on the sex chromosomes, differences in gene control due to differences in the sex-specific cellular environment, or more general differences in environmental exposures between the sexes.
Nutrient energy-dependent pheromone-controlled sex differences in the cell types of species from yeasts to humans link changes in the microRNA/messenger RNA balance and chromatin remodeling to learning and memory. Learning and memory links natural selection for codon usage and biophysically constrained RNA-mediated protein folding chemistry to chromosomal rearrangements. The detailed pathways that lead to the functional structure of supercoiled DNA link energy-dependent changes from angstroms to ecosystems in all living genera.
…viral latency is responsible for life-long pathogenesis and mortality risk…
Nutrient energy-dependent pheromone-controlled viral latency is the key to RNA-mediated healthy longevity. That fact has been revealed by serious scientists in publications across the past two decades. Pseudoscientists have refused to acknowledge the facts that refute their ridiculous theories. As always, however, the facts are irrefutable. That’s why they are called facts.
The amino acid optimality code (Fig 6) provides an alternative perspective on sequence changes between paralogs in evolution and human disease.
Parenthetically it is interesting to note even the yeast Saccharomyces cerevisiae has a gene-based equivalent of sexual orientation (i.e., a-factor and alpha-factor physiologies). These differences arise from different epigenetic modifications of an otherwise identical MAT locus (Runge and Zakian, 1996; Wu and Haber, 1995).
(2000) Organizational and activational effects of hormones on insect behavior (invertebrates)
(2014) Estrogen receptor α polymorphism in a species with alternative behavioral phenotypes (vertebrates)
(2014) RNA and dynamic nuclear organization (my comment)
As scientists, we should be interested in discovering and understanding the true sources of variation, which will be more informative in the development of clinical treatments.
(2016) Olfactory organ of Octopus vulgaris: morphology, plasticity, turnover and sensory characterization (all invertebrates and all vertebrates)
See for comparison: Jay R. Feierman
Variation is not nutrient availability and the something that is doing the selecting is not the individual organism. A feature of an educated person is to realize what they do not know. Sadly, you don’t know that you have an incorrect understanding [of] Darwinian biological evolution.
…the interactions between pre-mRNA and proteins fine-tune alternative splicing in a manner that can gradually create new protein functionalities without the need to create additional genes and without affecting existing proteins [4, 5, 6].
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.
For comparison to the energy-dependent de novo creation of new functional proteins via “…alternative splicings of otherwise identical genes” in the context of “…interactions between pre-mRNA and proteins…” that enables the fine-tuning of RNA-mediated cell type differentiation in species from microbes to humans, see:
Evolution by gene loss and Microbial Reconstitution Reverses Maternal Diet-Induced Social and Synaptic Deficits in Offspring
Oxytocin Levels Are Reduced in the Hypothalamus of MHFD Offspring
There is growing evidence that the neuropeptide oxytocin modulates numerous aspects of social behavior (Donaldson and Young, 2008) and is implicated in ASD (Lerer et al., 2008; Wu et al., 2005).
The antithetical conclusion that viruses link oxytocin to prairie vole monogamy and the evolution of human heterosexual love is not supported by any experimental evidence of biologically-based cause and effect that links energy-dependent changes to healthy longevity and virus-driven energy theft to all pathology.
See for comparison: