Conceptual critique: Innateness vs the death gene (1)

By: James V. Kohl | Published on: February 14, 2018

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Summary: The term innate is used in psychological explanations. The so-called explanations ignore facts about the light energy-dependent activation of endogenous substrates. The anti-entropic virucidal energy of sunlight links the endogenous substrates to biophysically constrained viral latency and healthy longevity via the physiology of reproduction in all living genera.

“Proximate mechanisms” and “evolution” are terms used by biologically uninformed theorists. That fact becomes perfectly clear in the context of The conceptual critique of innateness (paywalled)

One proposal is that innateness can be defined in terms of the biological property of environmental canalization. On this view, a trait is innate to the extent that it is developmentally buffered against a range of different environments. Another proposal is that innateness serves as an explanatory primitive for cognitive science. This view holds that there exist a sharp boundary between psychological and biological explanations and that to identify a trait as innate means that it falls into the latter explanatory domain.

For comparison to the sharp boundary between psychological and biological explanations, we eliminated the concept of innateness and claims about evolution from our 1996 Hormones and Behavior review of experience-dependent epigenetically- effected RNA-mediated cell type differentiation: From Fertilization to Adult Sexual Behavior.

See how our section on molecular epigenetics was linked from effects on hormones to the affects of hormones on behavior via alternative splicings of pre-mRNAs.

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…

Also, in an award-winning 2001 review, other co-authors helped to link energy-dependent top-down causation to biophysically constrained cause and effect via the affects of hormones on behavior. Epigenetic effects on hormones and affects on behavior are studied and integrated in the context of human ethology. See: Human pheromones: integrating neuroendocrinology and ethology

If you ignore the history of all published works on energy-dependent microRNA-mediated (aka pre-mRNA-mediated) top-down causation during the past two decades, you can continue to tout “evolution” as if it had any explanatory power. But it does not have any explanatory power whatsoever in the context of human ethology.

Simply put, “evolution” does not link epigenetic effects on hormones to the affect of hormones on behavior. Evolution, innate, and proximate mechanisms are terms used by biologically uninformed theorists whose ridicuous theories have no explanatory power.
See for comparison: Hormonal: The Hidden Intelligence of Hormones — How They Drive Desire, Shape Relationships, Influence Our Choices, and Make Us Wiser (Feb 13, 2018)
See for examples of explanatory power: pre mrna + alternative splicing and microRNA
Item: 1 of 69876 in today’s search at 9:23 AM Eastern Time A Genetic Network for Systemic RNA Silencing in Plants

Non-cell autonomous RNA silencing can spread from cell to cell and over long-distance in animals and plants.

That fact is commonly known among serious scientists. For comparison, pseudoscientists and other theorists also use the term “proximate mechanisms” outside the context of the links from the food energy-dependent non-cell autonomous RNA silencing and pheromone-controlled physiology of reproduction, which were obviously included in Darwin’s “conditions of life.” (Darwin’s “conditions of life” were bastardized by those who invented neo-Darwinian nonsense, and linked the nonsense to explanations of behavior in the context of human ethology.)

See for example: Jay R. Feierman is the antagonistic passive-aggressive moderator of the Human Ethology Yahoo Group.
After brief discussion of my claims in Nutrient-dependent/pheromone-controlled adaptive evolution: a model (2013), Jay R. Feierman reported this to the group:

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.

and this:

Jay R. Feierman: I am absolutely certain that if you showed this statement to any professor of biology or genetics in any accredited university anywhere in the world that 100% of them would say that “Random mutations are the substrate upon which directional natural selection acts” is a correct and true statement.

See for comparison: Small RNA pathways responsible for non-cell-autonomous regulation of plant reproduction (reported in the context of my “Sokalian Hoax” series (1-10).
K.I. Nonomura and others have since published EAT1 transcription factor, a non-cell-autonomous regulator of pollen production, activates meiotic small RNA biogenesis in rice anther tapetum (February 12, 2018)

ETERNAL TAPETUM1 (EAT1) is a basic-helix-loop-helix (bHLH) transcription factor indispensable for induction of programmed cell death (PCD) in postmeiotic anther tapetum, the somatic nursery for pollen production.

It links what organisms “eat” (get it?)to the physiology of pheromone-controlled reproduction in species from microbes to humans via the honeybee model organism and everything known about biophysically constrained viral latency. Theorists and other pseudoscientists, like Jay R. Feierman, must continue to live in fear that their nonsense will be exposed in the context of what might otherwise have become a culture war.
Instead, this group of Japanese researchers appears to have an unparalleled, albeit somewhat biophysically constrained, sense of humor. Sarcasm, for example, is often a humorous way to force pseudoscientists to recognize the facts they have ignored. It is somewhat the same as a rabbinical debate that starts with “You Fool!”
For example, You fool! The link from ETERNAL TAPETUM1 (EAT1) and/or what you eat to a basic biophysically constrained helix-loop-helix (bHLH) transcription factor and/or cell death can be placed into the context of how the death gene is activated by stress in all living genera.
See: Reduced expression of brain-enriched microRNAs in glioblastomas permits targeted regulation of a cell death gene
The reduced expression is caused by the virus-driven theft of quantized energy, which links nutrient stress and/or social stress from mutations to all pathology via the degradation of messenger RNA in species from archaea to humans.
Virus-mediated archaeal hecatomb in the deep seafloor

We show here for the first time the crucial role of viruses in controlling archaeal dynamics and therefore the functioning of deep-sea ecosystems, and suggest that virus-archaea interactions play a central role in global biogeochemical cycles.

See for comparison: The extent of codon usage bias in human RNA viruses and its evolutionary origin (2003)

Revealing the determinants of codon usage bias is central to the understanding of factors governing viral evolution.

Molecular Clocks and the Puzzle of RNA Virus Origins (2003)

…in the case of the primate lentiviruses, amino acid residues that are highly variable in HIV are sometimes conserved in chimpanzee SIV (19), and this may have a significant effect on dating estimates.

A Metagenomic Survey of Microbes in Honey Bee Colony Collapse Disorder (2007)

The observation that irradiated combs from affected colonies can be repopulated with naive bees suggests that infection may contribute to CCD.

Codon identity regulates mRNA stability and translation efficiency during the maternal-to-zygotic transition

The amino acid optimality code (Fig 6) provides an alternative perspective on sequence changes between paralogs in evolution and human disease.

Theorists have been repeatedly told told that there is no such thing as the emergence of the sun’s anti-entropic virucidal energy. They have also been repeatedly told there is no such thing as mutation-driven evolution. They have been warned that serious scientists have linked top-down causation to energy-dependent biophysically constrained viral latency. But, biologically uninformed theorists continue to ignore the facts about virus-driven pathology, and their ignorance will probably continue to cause the unnecessary suffering that leads to premature death, which may lead to the death of nearly everyone and everything on Earth.
Sudden emergence of human infections with H7N9 avian influenza A virus in Hubei province, central China (2018)

There have been five waves of H7N9 avian influenza virus (AIV) infection in humans since its initial emergence in China in 2013, posing a significant threat to public health. Hubei province was free local transmission during the first four waves of H7N9 AIV. However, multiple cases of human H7N9 infection were reported in Hubei during January 2017.

The emergence of influenza viruses has typically been constrained by ultraviolet light. This group of researchers recently presented their findings in that context.
Far-UVC light: A new tool to control the spread of airborne-mediated microbial diseases

This approach may help limit seasonal influenza epidemics, transmission of tuberculosis, as well as major pandemics.

The link from UV light to activation of the death gene and viral endemicity has been virtually ignored.
See also: Conceptual critique: Innateness vs the death gene (2)