“DNA methylation has become nearly synonymous with epigenetics,” says Brendan Hunt, an insect geneticist at the University of Georgia in Griffin. “This research brings needed attention to the importance of other epigenetics marks, like histone modifications.”
“We finally have a mechanism to understand ‘nurture’ in molecular terms,” says Gene Robinson, a geneticist at the University of Illinois, Urbana-Champaign, who studies caste determination in honey bees. The ant study, he adds, highlights “how the environment gets under the skin to affect gene expression, and consequently, neural activity and behavior.”
My comment: Gene Robinson’s word choice reveals the amount of nonsense he included in his claim that “We finally have a mechanism to understand ‘nurture’ in molecular terms…” His claim about “how the environment gets under the skin to affect gene expression” was placed into the context of epigenetic effects on genes and hormones that affect behavior by Bruce McEwen.
The authors note that on page 17184, right column, first paragraph, line 4, “effect” should instead appear as “affect.”
Robinson and McEwen know that we linked effect and affect in our 1996 Hormones and Behavior review in our section on molecular epigenetics. For example, Robinson, with Elekonich cited From Fertilization to Adult Sexual Behavior in Organizational and activational effects of hormones on insect behavior (2000).
Effects of hormones on brain and behavior occur through three mechanisms: (1) behaviors both organized and activated by hormones, (2) behaviors only organized by hormones, and (3) behaviors only activated by hormones (reviewed in Arnold and Breedlove, 1985; Diamond et al., 1996).”
My comment: In Diamond, Bintock and Kohl (1996), we detailed everything known about the molecular epigenetics of RNA-mediated cell type differentiation in species from microbes to mammals and linked it to chromosomal rearrangements and to sexual orientation.
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.
A potential ramification of epigenetic imprinting and alternative splicing may be occurring in Xq28, a chromosomal region implicated in homosexual orientation…
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).
My comment: The epigenetically-effected molecular mechanisms that link RNA-mediated cell type differentiation in yeasts to humans via every aspect of behavior including those associated with sexual orientation were placed into the context of brain gene expression in the honeybee.
See also: Brain gene expression changes elicited by peripheral vitellogenin knockdown in the honey bee (2013) Co-authored by Gene Robinson
Vitellogenin (Vg) is best known as a yolk protein precursor. Vg also functions to regulate behavioural maturation in adult honey bee workers, but the underlying molecular mechanisms by which it exerts this novel effect are largely unknown.
My comment: The yolk protein precursor links yeasts to invertebrates and egg-laying vertebrates, such as chickens via juvenile hormone (JH).
…the tight coregulatory relationship that exists between JH and Vg in the regulation of honey bee behavioural maturation is manifest at the genomic level and suggest that these two physiological factors act through common pathways to regulate brain gene expression and behaviour.
My comment: Taken together, Gene Robinson and others have linked our model of hormone-organized and hormone-activated differences in behavior from the nutrient-dependent pheromone-controlled behavior of yeasts and all invertebrates to all vertebrates via the honeybee model organism. This brings out model current in the context of our claims about pre-mRNAs, which are now also called microRNAs.
…we demonstrate a causal link between the Vg knockdown forager phenotype and variation in the abundance of microRNAs in different tissues with possible consequences for regulation of foraging behavior.
My comment: They demonstrate top-down causation linked from atoms to ecosystems to foraging behavior via the abundance of nutrient-dependent microRNAs in the different cell types of different tissues in different species. But they link the gene vitellogenin to an affect on microRNA regulation. They ignore everything known about epigenetics, metabolic networks, and genetic networks. They do not link atoms to ecosystems via the epigenetic effects of food odors and pheromones on the hormones that affect behavior.
The failure of researchers to link top-down causation to biologically-based cause and effect via any model that links atoms to ecosystems is catastrophic. It prevents others from understanding the difference between epigenetic effects on hormones and the affect of hormones on behavior in the context of all hormone-organized and hormone-activated behaviors in all vertebrates and invertebrates.
Their failure becomes evident in this report: Role of olfaction in Octopus vulgaris reproduction. This link opens the pdf
Future work on O. vulgaris olfaction must also consider how animals acquire the odours detected by the olfactory organ and what kind of odour the olfactory organ perceives. The OL acting as control centre may be target organ for metabolic hormones such as leptin like and insulin like peptides, and olfactory organ could exert regulatory action on the OL via epigenetic effects of nutrients and pheromones on gene expression (Kohl, 2013; Elekonich and Robinson, 2000). — p. 61
My comment: I find it difficult to believe that only one group of researchers would link two decades of my published works from atoms to ecosystems in all living genera. However, others have virtually ignored the fact that we were the first to link the molecular mechanisms of all RNA-mediated cell type differentiation in our 1996 Hormones and Behavior review. Lest anyone think I am complaining about being ignored in the context of “sour grapes,” let’s look at the other links from atoms to ecosystems that Gene Robinson and others have ignored.
Until recently, transduction of antibiotic resistance via phage was assumed to be a very minor source of the spread of resistance, said Hilbert. “New information from the sequencing of bacterial DNA has shown that transduction must be a driving force in bacterial evolution, and thus, quite common.”
My comment: The claim that virus-driven “…antibiotic resistance via phage was assumed to be a very minor source of the spread of resistance…” can be linked to assumptions by neo-Darwinian theorists that antibiotic resistance was caused by mutations, which caused the evolution of one species from another. Those claims are not supported by any experimental evidence that links atoms to ecosystems or any that link what is known to serious scientists about biologically-based cause and effect.
Neo-Darwinian theorists fail to acknowledge what is known to all serious scientists about the molecular epigenetics of nutrient-dependent microRNA-mediated cause and effect. They ignore everything known about virus-driven genomic entropy. Nutrient energy-dependent DNA repair obviously occurs only in the context of nutrient-dependent microRNAs. The nutrient-dependent microRNAs are linked from energy-dependent base pair substitutions to RNA-mediated amino acid substitutions. The beneficial RNA-mediated amino acid substitutions are fixed in the context of the physiology of reproduction. The substitutions link microRNAs and adhesion proteins to supercoiled DNA. The supercoiled DNA protects organized genomes from virus-driven entropy in species from bacteria to all invertebrates and vertebrates.