Energy-dependent autophagy links food odors and pheromones from the innate immune system and RNA-mediated feedback loops to the physiology of reproduction in all living genera via chromosomal inheritance. Transgenerational epigenetic inheritance is nutrient-energy-dependent and pheromone-controlled.
That fact has been established in the extant literature since 1933, when Thomas Hunt Morgan won the Nobel Prize in Medicine, and Erwin Schrodinger shared the 1933 Prize in Physics with Paul A.M. Dirac.
See for example: From Fertilization to Adult Sexual Behavior December 1996
Research has established the broad mammalian developmental plan that genes on the sex chromosomes influence gonad development which determines gonadal hormone production (or its absence) leading to modification of the genitalia and simultaneously biasing the nervous system to organize adult sexual behavior. This might be considered the “gonad to hormones to behavior” model. It is clear, however, that although this model generally works well it is incomplete. The model does not account for behavioral influences attributed to the environment or to genetic but nongonadal or hormonal factors. In this essay we probe those areas of sexual development that are neither differentiated by hormones nor activated by them. The concept of the environment used for our discussion is very broad; it incorporates considerations of both the molar and the molecular levels. The general sense of the word “environment” as something exterior to the person is retained, even if that something influences intraperson processes. In addition, we focus directly on molecular events themselves. Here the “environment” involved can be that within a DNA segment. We also expand the notion of “biologically based sex differences.” Although many, and perhaps most, important sex differences arise from gonadal and hormonal development, also important are sex differences which are neither gonadal nor hormonal. All these factors affect the internal workings of the individual and intervene in structuring how the social environment might or might not modify sexual behavior. This discourse calls attention to features that are central to the so-called nature-nurture discussion.
My Synopsis: Nutrient energy-dependent pheromone-controlled changes in RNA-mediated events link experimental evidence of biologically-based cause and effect from nature and nurture to differences in morphological and behavioral phenotypes.
Structural Brain Network Reorganization and Social Cognition Related to Adverse Perinatal Condition from Infancy to Early Adolescence December 2016
Brain development consists of a genetically controlled but environmentally modulated complex process starting early in fetal life, which makes it very sensitive to adverse intrauterine environment and/or to a premature exposure to extrauterine medium. Alterations in fetal brain development can result in long-term structural brain reorganization as well as in social cognition impairments in childhood and adolescence (Leitner et al., 2000; Wiles et al., 2006; Baschat, 2011; Guellec et al., 2011). Namely, intrauterine growth restriction (IUGR), a condition affecting 5–10% of all pregnancies involving a decrease in the amount of nutrients and oxygen arriving to the fetus, has consequences on the developing brain associated to short- and long-term impairments in both brain function and structure (Rees et al., 2008; Levine et al., 2015).
Discussion (excerpt):
Brain connectivity evolves during development, starting prenatally and continuing into adolescence (Hagmann et al., 2010; Yap et al., 2011; Dennis and Thompson, 2013; Ball et al., 2014; Dubois et al., 2014).
Conclusion:
These structural differences are related to a higher risk of social cognitive disorders in IUGR, being especially relevant the association with executive dysfunction and hyperactivity/inattention behavior.
My Synopsis: Nutrient energy-dependent pheromone-controlled changes in RNA-mediated events link experimental evidence of biologically-based cause and effect from nature and nurture to differences in morphological and behavioral phenotypes.
The reason there is no difference between my synopsis of our 1996 review and my synopsis of the article from 2016 is clear. In our review, the changes from fertilization to adults are nutrient-dependent and pheromone-controlled via the physiology of reproduction and transgenerational epigenetic inheritance of species-specific changes during the development of all morphological and behavioral phenotypes in species from microbes to humans.
The difference in the 2016 report is the claim that species-specific differences “evolve.” No experimental evidence of biologically based cause and effect suggests that any differences in cell types in any individual of any species “evolve.” Ecological variation must be linked from conserved molecular mechanisms of energy-dependent cell type differentiation to ecological adaptation. That cannot be done via theories of evolution.
See for instance: Mutation-Driven Evolution Jun 14, 2013
See for comparison: Nutrient-dependent/pheromone-controlled adaptive evolution: a model Jun 14, 2013
See also: Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems (2014)
See: DNA Damage
See also: Combining CNV and SNV Detection in a Single Test: An Alternative to Whole-Genome Sequencing (December 13, 2016)
This webinar will discuss a genomic strategy that detects single nucleotide variants and copy number variants in a single assay. This approach serves as a cost-effective alternative to whole-genome sequencing and shows promise for the field of cytogenetics.
This webinar will discuss a genomic strategy that detects single nucleotide variants and copy number variants in a single assay. This approach serves as a cost-effective alternative to whole-genome sequencing and shows promise for the field of cytogenetics.
Humans also have various pheromone-induced physiological effects, especially those associated with reproduction [46, 47]. This suggests that the human olfactory system is still an effective pathway for influencing environmental factors on the human nervous system. Various psychoemotional states of the human nervous system can, in turn, disrupt the integrity of the chromosomal apparatus of target cells, for instance lymphocytes [41, 42]. Therefore, studies on the oppositely directional modulation of the mutagenic consequences of stress in rodents with the use of specific, volatile, and zoosocial important chemosignals are a promising approach both to modeling posttraumatic stress disorders in humans [36] and to searching for mehods of their treatment.
[46] is Kohl, J.V., Atzmueller, M., Fink, B., and Grammer, K., Human pheromones: integrating neuroendocrinology and ethology, Neuroendocrinol. Lett., 2001, vol. 22, pp. 309–321.
The fact that “chemosignals” have an antimutagenic effect links pheromones to anti-entropic epigenetic effects on cell type differentiation via the conserved molecular mechanisms that link food odors to all energy-dependent healthy longevity.
See: Feedback loops link odor and pheromone signaling with reproduction
See also: Combating Evolution to Fight Disease
…an important gap is being filled by molecular understanding of the genesis of variation that confers the ability to evolve.
See also, my comments and the comment by Robert Frye on: Combating Evolution to Fight Disease
Re: “Molecular biology and evolutionary biology have been separate disciplines and scientific cultures: The former is mechanistic and focused on molecules; the latter is theoretical and focused on populations.”Now see: A mechanistic link between gene regulation and genome architecture in mammalian developmenthttp://www.sciencedirect.com/science/article/pii/S0959437X14000495 for the refutation of neo-Darwinian pseudoscientific nonsense.Experimental evidence of biologically-based cause and effect does not support ideas about mutations, natural selection, and the evolution of biodiversity.Experimental evidence of biologically-based cause and effect supports the fact that ecological variation leads to nutrient-dependent pheromone-controlled ecological adaptations in species from microbes to man via conserved molecular mechanisms.
Submitted on Tue, 07/15/2014 – 22:13
I am concerned at the lack of understanding of basic evolutionary processes in the Perspective of Rosenberg and Queitsch. They assert that a cornerstone assumption of evolution is that mutations are ‘the sole drivers of evolution’. That is nonsense as the driver of evolution is not mutations or variation but selection, be it natural, artificial, kin or sexual selection. Mutation is but one of the factors that contribute to variation. In addition, we have known for a long time that mutations are not solely random, constant or gradual. I seem to remember from high school biology (1960’s) that the environment can effect mutation rates through heat, chemicals and radiation. Does the editorial process of Science not include Perspectives?
Submitted on Mon, 03/17/2014 – 14:28
James V. Kohl
See for comparison: UV-Induced Charge Transfer States in DNA Promote Sequence Selective Self-Repair
DNA damage repair is energy-dependent. The speed of light on contact with water must link quantized energy to DNA damage because an anti-entropic energy source is required For example, the virucidal anti-tropic effects of ultraviolet light on RNA-mediated protein folding chemistry link the innate immune system to supercoiled DNA via autophagy and the physiology of reproduction.
Supercoiled DNA protects organized genomes from virus-driven energy theft. RNA-mediated amino acid substitutions link the nutrient-dependent pheromone-controlled physiology of reproduction from supercoiled DNA to healthy longevity. Virus-driven energy theft links mutations to all pathology.
The field of cytogenetics links energy-dependent changes in the microRNA/messenger RNA balance from single nucleotide variations (SNVs) to copy number variations (CNVs) in all cell types. Virus-driven energy theft will continue to be linked to healthy longevity and all biodiversity via single nucleotide polymorphisms (SNPs) and natural translational selection for codon optimality. Virus-driven energy theft will continue to be linked from energy-dependent viral latency to all pathology.