5th-6th Sept 2018 Dublin, Ireland

The eternal significance of microRNAs (8)

Use of definitions in attempts to explain any aspect of species-specific biophysically constrained cell type differentiation and aging has been replaced by the use of model systems of biological processes.  Biological processes can be compared to so-called “evolutionary processes” to show that only biological processes need to be considered in the context of Darwin’s “conditions of life” or answers to the the question  What is Life? Schrödinger (1944).
K. L. Mettinger et al. (eds.), Exosomes, Stem Cells and MicroRNA, Advances in Experimental Medicine and Biology 1056, https://doi.org/10.1007/978-3-319-74470-4_6

This volume provides insight into the pivotal roles of stem cells, exosomes and other microvesicles in biofunction and molecular mechanisms and their therapeutic potential in translational nanomedicine. It further highlights evidence from recent studies as to how stem cell derived exosomes and microRNAs may restore and maintain tissue homeostasis, enable cells to recover critical cellular functions and begin repair regeneration.

Chapter 2 The Emerging Roles of microRNAs in Stem Cell Aging

involved in many biological processes such as developmental timing, differentiation, cell death, stem cell proliferation and differentiation, immune response, aging and cancer. Accumulating studies in recent years suggest that miRNAs play crucial roles in stem cell division and differentiation. In the present chapter, we present a brief overview of these studies and discuss their contributions toward our understanding of the importance of miRNAs in normal and aged stem cell function in various model systems.

Chapter 6  MicroRNAs, Regulatory Messengers Inside and Outside Cancer Cells

…like hormones, miRNAs can be secreted and regulate gene expression in recipient cells. Altered expression levels of miRNAs in cancer cells determine the acquisition of fundamental biological capabilities (hallmarks of cancer) responsible for the development and progression of the disease.

Model systems link the energy-dependent creation of microRNAs from microRNA biogenesis to the regulation of all cancer hallmarks. The virus-driven degradation of messenger RNA has been linked to all cancers and all other pathology in species from microbes to humans. Natural selection for energy-dependent codon optimality has been linked to healthy longevity.
See: Codon identity regulates mRNA stability and translation efficiency during the maternal-to-zygotic transition
See for comparison:  The Neutral Theory in Light of Natural Selection May 2, 2018

…50 years after its introduction by Kimura. We argue that the neutral theory was supported by unreliable theoretical and empirical evidence from the beginning, and that in light of modern, genome-scale data, we can firmly reject its universality. The ubiquity of adaptive variation both within and between species means that a more comprehensive theory of molecular evolution must be sought.

The ubiquity of adaptive variation attests to the facts about how the creation of quantized energy is linked to biophysically constrained viral latency. Adaptive variation links energy-dependent changes from angstroms to ecosystems in all living genera  via the physiology of their food energy-dependent pheromone-controlled reproduction.

For comparison to mRNA stability during the maternal-to-zygotic transition, see: Oppositional COMT Val158Met effects on resting state functional connectivity in adolescents and adults

The energy-dependent molecular mechanisms of recombination clearly link microRNA biogenesis to the stability of organized genomes during the life histories of all genera. Serious scientists object to the use of definitions in attempts to explain any aspect of species-specific biophysically constrained cell type differentiation.

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

…it is tiresome to raise the same objections repeatedly, wondering why researchers have not fulfilled some of the basic requirements for establishing the occurrence of an autophagic process.

 

Cases of Cytosis

Autophagy.pro vs Nature Publications Group

Autophagy is the antiphage defense strategy (James V. Kohl: December 8, 2016)

Autophagy.pro was launched on 11 December 2017

See for comparison from the Nature Publications Group.  First, they try to establish a more complicated new definition with several different pathways

Autophagy

Autophagy is a process by which cellular material is degraded by lysosomes or vacuoles and recycled. Several autophagy pathways operate within a cell, including macroautophagy, microautophagy and chaperone-mediated autophagy.

After the new definition, and the extension of vague processes and magical pathways to macroautophagy, microautophagy and chaperone-mediated autophagy, we see:

Latest Research and Reviews

An and Harper quantify ribophagy in mammalian cells and show that nutrient-deprivation-induced ribophagy is independent of the ATG8 conjugation system, whereas proteotoxic stress-induced ribophagy requires ATG5 and VPS34.

The similarities and differences between the energy-dependent changes in epigenetic effects of nutrient stress and the epigenetic effects of social stress has not been addressed in published works until recently. But see: microRNA Items: 1 to 20 of 67725.
See for comparison: ribophagy Items: 1 to 20 of 29
Food energy-dependent changes in the microRNA/messenger RNA balance biophysically constrain viral latency in species from microbes to humans. The virus-driven degradation of messenger RNA has been linked to all pathology. The “Nature Publications Group” tries to sneak up from behind with the less detailed link from ribophagy to autophagy.
Research | 11 December 2017
Systematic analysis of ribophagy in human cells reveals bystander flux during selective autophagy

Research | 11 December 2017 | open
SPLICS: a split green fluorescent protein-based contact site sensor for narrow and wide heterotypic organelle juxtaposition
Research | 11 December 2017
Autophagy induced during apoptosis degrades mitochondria and inhibits type I interferon secretion
Research | 11 December 2017 | open
RAB37 interacts directly with ATG5 and promotes autophagosome formation via regulating ATG5-12-16 complex assembly
Sour grapes?

Nobody wants to belong to the party of losers. One of the best strategies in such a case is evidently an interpretation of the change as a gradual accumulation of knowledge while their work has always been at the cutting edge. — Kalevi Kull

The losers at the “Nature Publications Group” banned me from commenting on any article (~two years ago). Predictably, the “Nature Publications Group” and all others will be forced to link the virus-driven degradation of messenger RNA to all pathology and eliminate the pseudoscientific nonsense touted by neo-Darwinian theorists and “Big Bang” cosmologists.
See also:  Journal of Genetics and DNA Research Articles in Press | Volume 1, Issue 1
The Gene Polymorphism of VMAT2 Decrease the Risk of Developing SCZ in Male Han Chinese
Biophysical and Biochemical Mechanisms of Forming and Development A Human Eukaryotic Organism from Single Pluripotent Cell into Multicellular Embryo and A Living Organism in Norm
Mouse Models for NASH: Are we there yet?
Are we All Transgenic?
Genetic Engineering 2020
On Novel Anti-viral HIV Gene Editing Platforms
2016 – 2017 Historical context:
MicroRNAs and Autophagy: Fine Players in the Control of Chondrocyte Homeostatic Activities in Osteoarthritis
Emerging connections between RNA and autophagy
I founded the domains Pheromones.com (1995), RNA-mediated.com (2015) and Autophagy.pro (2017) because the food energy-dependent species-specific production of pheromones clearly links feedback loops to all biophysically constrained RNA-mediated biodiversity via autophagy.
 
 

Alternative splicing of pre-mRNA

Epigenetic facts vs variable recombination theories

6/14/13 Nutrient-dependent/pheromone-controlled adaptive evolution: a model

….the model represented here is consistent with what is known about the epigenetic effects of ecologically important nutrients and pheromones on the adaptively evolved behavior of species from microbes to man. Minimally, this model can be compared to any other factual representations of epigenesis and epistasis for determination of the best scientific ‘fit’.

7/25/13
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.
7/26/13
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.

Facts:

Epigenetic modifications poster
DNA repair pathways poster
Epigenetic Dynamics in Stem Cells and Differentiation webinar
Epigenetic Editing: Permanently Modulate Gene Expression webinar
Histone modifications: a guide
Epigenetic Mechanisms in Early Mammalian Development webinar
DNA Methylation Changes During Cell Differentiation webinar
Chromatin: from nucleosomes to chromosomes
Epigenetics round-up of 2014

Changes in histone acetylation may aid memory reconsolidation in post-traumatic stress disorder

See also: Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems (2014)

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. Species diversity is a biologically-based nutrient-dependent morphological fact and species-specific pheromones control the physiology of reproduction. The reciprocal relationships of species-typical nutrient-dependent morphological and behavioral diversity are enabled by pheromone-controlled reproduction. Ecological variations and biophysically constrained natural selection of nutrients cause the behaviors that enable ecological adaptations. Species diversity is ecologically validated proof-of-concept. Ideas from population genetics, which exclude ecological factors, are integrated with an experimental evidence-based approach that establishes what is currently known. This is known: Olfactory/pheromonal input links food odors and social odors from the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man during their development.

Theme issue ‘Evolutionary causes and consequences of recombination rate variation in sexual organisms’ (2017)
Recombination rate variation in sexual organisms is energy-dependent and RNA-mediated. Variation is biophysically constrained by the pheromone-controlled physiology of reproduction in species from microbes to humans. See: From Fertilization to Adult Sexual Behavior (1996)

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.
A potential ramification of epigenetic imprinting and alternative splicing may be occurring in Xq28, a chromosomal region implicated in homosexual orientation (Brook, 1993; Hu, Pattatucci, Patterson, Li, Fulker, Cherny, Kruglyak, and Hamer, 1995; Turner, 1995). Xq28 contains one of the X chromosome’s two pseudoautosomal regions (PARs), adjoins the telomere, and has various means of gene expression control (D’Esposito, Ciccodicola, Gianfrancesco, Esposito, Flagiello, Mazzarella, Schiessinger, and D’Urso (1996). Xq28, therefore, is a chromosomal region that has many of the heterochromatic and telomeric characteristics that participate in sexual determination and behavior in other species.

Theories:

Review article: Variation in recombination frequency and distribution across eukaryotes: patterns and processes
Jessica Stapley, Philine G. D. Feulner, Susan E. Johnston, Anna W. Santure and Carole M. Smadja
Phil. Trans. R. Soc. B December 19, 2017 372 20160455; doi:10.1098/rstb.2016.0455
http://rstb.royalsocietypublishing.org/content/372/1736/20160455
Review article: The impact of recombination on human mutation load and disease
Isabel Alves, Armande Ang Houle, Julie G. Hussin and Philip Awadalla
Phil. Trans. R. Soc. B December 19, 2017 372 20160465; doi:10.1098/rstb.2016.0465
http://rstb.royalsocietypublishing.org/content/372/1736/20160465
Opinion piece: Connecting theory and data to understand recombination rate evolution
Amy L. Dapper and Bret A. Payseur
Phil. Trans. R. Soc. B December 19, 2017 372 20160469; doi:10.1098/rstb.2016.0469
http://rstb.royalsocietypublishing.org/content/372/1736/20160469
Review article: Coevolution between transposable elements and recombination
Tyler V. Kent, Jasmina Uzunović and Stephen I. Wright
Phil. Trans. R. Soc. B December 19, 2017 372 20160458; doi:10.1098/rstb.2016.0458
http://rstb.royalsocietypublishing.org/content/372/1736/20160458
Review article: Evolution of recombination rates between sex chromosomes
Deborah Charlesworth
Phil. Trans. R. Soc. B December 19, 2017 372 20160456; doi:10.1098/rstb.2016.0456
http://rstb.royalsocietypublishing.org/content/372/1736/20160456
Research article: Low recombination rates in sexual species and sex–asex transitions
Christoph R. Haag, Loukas Theodosiou, Roula Zahab and Thomas Lenormand
Phil. Trans. R. Soc. B December 19, 2017 372 20160461; doi:10.1098/rstb.2016.0461
http://rstb.royalsocietypublishing.org/content/372/1736/20160461
(openaccess) Review article: The consequences of sequence erosion in the evolution of recombination hotspots
Irene Tiemann-Boege, Theresa Schwarz, Yasmin Striedner and Angelika Heissl
Phil. Trans. R. Soc. B December 19, 2017 372 20160462; doi:10.1098/rstb.2016.0462
http://rstb.royalsocietypublishing.org/content/372/1736/20160462
(openaccess) Research article: The Red Queen model of recombination hot-spot evolution: a theoretical investigation
Thibault Latrille, Laurent Duret and Nicolas Lartillot
Phil. Trans. R. Soc. B December 19, 2017 372 20160463; doi:10.1098/rstb.2016.0463
http://rstb.royalsocietypublishing.org/content/372/1736/20160463
(openaccess) Research article: Background selection as null hypothesis in population genomics: insights and challenges from Drosophila studies
Josep M. Comeron
Phil. Trans. R. Soc. B December 19, 2017 372 20160471; doi:10.1098/rstb.2016.0471
http://rstb.royalsocietypublishing.org/content/372/1736/20160471
(openaccess) Review article: Recombination rate plasticity: revealing mechanisms by design
Laurie S. Stevison, Stephen Sefick, Chase Rushton and Rita M. Graze
Phil. Trans. R. Soc. B December 19, 2017 372 20160459; doi:10.1098/rstb.2016.0459
http://rstb.royalsocietypublishing.org/content/372/1736/20160459
(openaccess) Review article: Are the effects of elevated temperature on meiotic recombination and thermotolerance linked via the axis and synaptonemal complex?
Christopher H. Morgan, Huakun Zhang and Kirsten Bomblies
Phil. Trans. R. Soc. B December 19, 2017 372 20160470; doi:10.1098/rstb.2016.0470
http://rstb.royalsocietypublishing.org/content/372/1736/20160470
Research article: What drives the evolution of condition-dependent recombination in diploids? Some insights from simulation modelling
Sviatoslav R. Rybnikov, Zeev M. Frenkel and Abraham B. Korol
Phil. Trans. R. Soc. B December 19, 2017 372 20160460; doi:10.1098/rstb.2016.0460
http://rstb.royalsocietypublishing.org/content/372/1736/20160460

Cytosis can be used to teach everything from base editing to RNA editing to everyone over age 10. They will learn how to link the creation of energy to biophysically constrained viral latency via the physiology of pheromone-controlled reproduction.

Pheromones biophysically constrain RNA-mediated biodiversity (1)

Elaine Morgan on paradigm shifts. Her view of the pseudoscientific nonsense touted by neo-Darwinian theorists and “Big Bang” cosmologists is humorous and she accurately represents what’s been happening to me and others like me for the past two decades. It’s what we expect. It’s your choice to keep laughing about it.

See for comparison: Functional screening in human cardiac organoids reveals a metabolic mechanism for cardiomyocyte cell cycle arrest
Reported as: Scientists have identified the metabolic pathway associated with heart repair

Scientists identified the pathway using experiments performed on engineered heart tissues grown from stem cells. Following a study that mapped the pathways found in mouse hearts, this new study correlated those pathways to the human heart, identifying the specific pathway in human heart tissues. By profiling and comparing heart with and without regeneration capacity, the specific pathway was isolated.

See also: Metabolism switch signals end for healing hearts

Dr Hudson’s team is now working with a company to identify drugs that could re-activate the heart’s ability to self-repair.

The pathway is food energy-dependent and RNA-mediated. That fact is obvious and it attests to the fact that the pathway is biophysically constrained by the pheromone-controlled physiology of reproduction, which links the fixation of amino acid substitutions to healthy longevity in all living genera. Drug therapies typically do not lead to fixation of amino acid substitutions or to healthy longevity.
For comparison, see: Assessment of Pep, Fndc5, C2c12, Pgc1α Pattern of Genes Expression during Differentiation of Human Embryonic Stem Cells into Heart Cells

The mouse embryonic stem cells as a model for cardiac differentiation induced by ascorbic acid used and the pattern of expression of PEP at certain stages of differentiation were analyzed by Real-Time PCR technique.

This suggests ascorbic acid (vitamin C) may be essential for the biophysical constraints on the creation of amino acids that differentiate cell types. But see: A universal trend of amino acid gain and loss in protein evolution

Amino acid composition of proteins varies substantially between taxa and, thus, can evolve.

For contrast to the claim the amino acid compositions evolve see:
Figures 1-3 are examples of what is known about learning and memory in the context of brain waves and everything else known about energy-dependent biophysically constrained RNA-mediated cell type differentiation.
Figure 1: The amino acid sequence encoded by the gene FNDC5.
Figure 2: Structure of N-terminal and C-terminal gene FNDC5 the region.
Figure 3: How FNDC5 gene and PGC1a neuron in the human brain functions.
In an invited review of nutritional epigenetics, I linked exogenous vitamin C to levels of endogenous vitamin C and differences in the amino acid sequence to human brain functions via the food energy-dependent pheromone-controlled physiology of reproduction in a population of modern humans in Central China.
See: Sago-Type Palms Were an Important Plant Food Prior to Rice in Southern Subtropical China
See also: Stability of bioactive compounds in butiá (Butia odorata) fruit pulp and nectar

Pulp pasteurization resulted in a reduction in phenolic, flavonoid, carotenoid, and ascorbic acid contents.

If the ascorbic acid/vitamin C content of “Sago-Type Palms” was not reduced by pasteurization, Vitamin C and phenolic, flavonoid, carotenoid would be the most likely link from the anti-entropic virucidal energy of sunlight to plant microRNAs, which helped to stabilize the energy-dependent microRNA/messenger RNA balance in specific human populations. Vitamin C in one population. Phenolics, flavonoids and or carotenoids et al., in others.
In all cases, all populations must eat to reproduce. Dietary phytochemicals have repeatedly been linked to biophysically constrained viral latency by constraints on cell type differentiation.
See also: Regulation of microRNA using promising dietary phytochemicals: Possible preventive and treatment option of malignant mesothelioma.
I typically do not use “case studies” to explain biologically-based cause and effect. However, there are two probable outcomes linked to the two cases of Cytosis that I purchased:

Pathology: An abnormal increase in the number of undifferentiated cell types

Energy-dependent biophysically constrained viral latency: (aka biologically-based healthy longevity) in the context of the energy-dependent movement of cells between parts of organisms

The link from the creation of sunlight to the creation of ATP and the creation of RNA should be clear to all serious scientists. The link from the anti-entropic virucidal energy of sunlight to biophysically constrained viral latency should be equally clear to anyone who plays the cell biology game “Cytosis” and to anyone who reads this review of nutritional epigenetics.

Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems

Conclusion:

Nutrient-dependent pheromone-controlled ecological adaptations exemplify how sensing nutrients and secreting the metabolites of nutrients accomplishes different tasks. Efficient circuits enable the functional flexibility that is required in ever-changing ecologies that cause species diversity. Biophysical constraints on ecological adaptations are exemplified in physical proof which suggests that Kohl’s Laws of Biology (Kohl’s Laws) represent what Darwin called ‘conditions of life.’

Physical proof of species diversity links ecological variations from nutritional epigenetics to 1) biophysically constrained protein folding via 2) atomic level changes in base pairs (i.e., the nucleotides of DNA); 3) amino acid substitutions; 4) changes in the miRNA/mRNA balance; 5) the metabolism of nutrients to species-specific pheromones that 6) control the physiology of reproduction, and 7) chromosomal rearrangements that link the reciprocity of these interactions to the morphological and behavioral phenotypes manifested in species diversity. Across-species examples of biologically plausible ecologically validated cause and effect link the physical proof from conserved molecular mechanisms of DNA uptake that extends these representations of nutrient-dependent epigenetic effects to differences in pheromone-controlled morphological and behavioral human phenotypes.

The plausibility and ecological validity of Kohl’s Laws in the context of Darwin’s ‘conditions of life’ can be compared to theories about biologically-based cause and effect in the context of species diversity. In mammals, for example, the explanatory power of a model of ecological variation and biophysically constrained nutrient-dependent pheromone-controlled ecological adaptations became clear with companion papers published in 2013. See for review [30].

The companion papers [162-163] told a new short story of ecological adaptations. In the context of climate change and changes in diet, the story began with what probably was a nutrient-dependent base pair change and a variant epiallele that arose in a human population in what is now central China. Apparently, the effect of the epiallele was adaptive and it was manifested in the context of an effect on sweat, skin, hair, and teeth. In another mammal, such as the mouse, the effect on sweat, skin, hair, and teeth is probably due to a nutrient-dependent epigenetic effect on hormones responsible for the tweaking of immense gene networks that metabolize nutrients to pheromones. The pheromones appear to control the nutrient-dependent epigenetically-effected hormone-dependent organization and hormone-activation of reproductive sexual behavior in mammals such as mice and humans, but also in invertebrates and in microbes as previously indicated.

The ecological adaptations, which appear to be manifested in the human population are detailed in these two reports [162-163]. The ecological adaptations are likely to be nutrient-dependent and pheromone-controlled. If so, ecological variation probably leads to ecological, social, neurogenic, and socio-cognitive niche construction, which is manifested in increasing organismal complexity and species diversity. If not, there may be something as yet unknown about mutations and evolution that makes sense in the light of what is known about nutritional epigenetics and the molecular biology of species from microbes to man.

 

fruit-dove

Theories vs facts about polycombic adaptation

See: Demoncrats fight polycombic ecological adaptation

Exosomes as miRNA Carriers: Formation–Function–Future

Important aspects will be highlighted as a take-home message (THM) at the end of each paragraph.

THM: Extracellular vesicles transport miRNA in a paracrine and endocrine manner. Questions regarding the cellular options of producing either microvesicles or exosomes and their difference in miRNA composition and number are still unknown.

In my 2014 invited review, the four F’s, Formation–Function–Future and Copulation were included in details about how the nutrient energy-dependent de novo creation of microRNAs must be linked to nutritional epigenetics. My invited review was returned without review by the guest editors of a special issue of “Nutrients.”
I realized the guest editors had “baited me” into providing them with all the available current information and published my submission to Figshare. That’s how I show the level of deception that biologically uninformed theorists still use to obfuscate what is known to serious scientists about biologically-based cause and effect.

See for example: Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems (April 10, 2014)

Abstract: “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. Species diversity is a biologically-based nutrient-dependent morphological fact and species-specific pheromones control the physiology of reproduction. The reciprocal relationships of species-typical nutrient-dependent morphological and behavioral diversity are enabled by pheromone-controlled reproduction. Ecological variations and biophysically constrained natural selection of nutrients cause the behaviors that enable ecological adaptations. Species diversity is ecologically validated proof-of-concept. Ideas from population genetics, which exclude ecological factors, are integrated with an experimental evidence-based approach that establishes what is currently known. This is known: Olfactory/pheromonal input links food odors and social odors from the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man during their development.”

Lynnette Ferguson, was one of two guest editors that invited my review.
 
She is the co-author of The Interaction between Epigenetics, Nutrition and the Development of Cancer This article belongs to the Special Issue NutritionalEpigenetics
 

Conclusion:

…it is imperative to understand the implications of diet on epigenetic modifications, and the effect of those modifications on the development of cancer today and in future generations. Such an understanding and an appropriate resultant response would help decrease the level of risk in future generations.

There would be no future generations if diet could not be epigenetically linked from metabolism to the pheromones that control the physiology of reproduction in species from microbes to human via energy-dependent changes in the microRNA/messenger RNA balance. The microRNA/messenger RNA balance biophysically contrains RNA-mediated protein folding chemistry.

Protein folding chemistry links energy-dependent changes from angstroms to ecosystems in all living genera via the innate immune system and fixation of RNA-mediated amino acid substitutions in supercoiled DNA. Supercoiled DNA exemplifies natural section for energy-dependent codon optimality, but theorists will not accept that fact. They would rather believe that the mutations in DNA are naturally selected and that mutation-driven evolution automagically occurs outside the context of energy or the virus-driven energy theft that causes all mutations and all pathology.

See also: The developmental basis for the recurrent evolution of deuterostomy and protostomy

This scenario challenges the assumed value of extant blastoporal behaviours for explaining the evolutionary origin and diversification of Bilateria that has been presumed for over 100 years4,5,6,7,9,10,11. Freeing the constraint that the mouth and anus have a necessary association with the embryonic blastopore will help in understanding the developmental events underlying the evolution of an alimentary canal5,20,21,50, and ultimately the appearance and diversification of bilaterian body plans.

All scenarios that failed to link energy-dependent behavior to the physiology of reproduction and also failed to link virus-driven energy theft to all pathology have always been based on questionable assumptions. The assumptions fall outside the context of Darwin’s “conditions of life,” which require links from what organisms eat to signaling and sensing and the behavior of other organisms.

For example, Schrodinger (1944) linked excretion from mammals to sunlight as the source of anti-entropic virucidal energy used to support all ecosystems. All serious scientists have done that since Thomas Hunt Morgan won the 1933 Nobel Prize in Physiology or Medicine for linking chromosomes to transgenerational epigenetic inheritance long before most people understood what the term autophagy means.

rp_levels-of-organization.jpg

Energy-dependent maternal-to-zygotic transition

Small Non-coding RNAs Associated with Viral Infectious Diseases of Veterinary Importance: Potential Clinical Applications
ON 11/14/16 The co-author Mohamed Samir wrote: 

Because our article is among the top 25% most viewed and downloaded articles in the third quarter of 2016 in “Frontiers in Veterinary Science”, The editor of the journal has invited me to host and moderate a new research topic in his journal about miRNAs in veterinary filed. Thanks God.

The topic is virtually guaranteed to bring out the best in researchers who have already linked energy-dependent changes from angstroms to ecosystems in all genera via animal models that make it clear that virus-driven energy theft causes all pathology.
See also: Codon identity regulates mRNA stability and translation efficiency during the maternal-to-zygotic transition

The bias between codons or amino acids, and mRNA expression levels has been previously recognized across species and is thought to result from selection for efficient, accurate translation, and folding of highly expressed genes (Ikemura, 1982; Akashi, 1994; Akashi & Gojobori, 2002; Drummond & Wilke, 2008; Kudla et al, 2009; Novoa & Ribas de Pouplana, 2012). The amino acid optimality code (Fig 6) provides an alternative perspective on sequence changes between paralogs in evolution and human disease.

See also: RNA Structural Modules Control the Rate and Pathway of RNA Folding and Assembly
Natural selection for codon optimality is an energy-dependent biophysically constrained RNA-mediated sexually differentiated biological function that has been linked to RNA folding and the assembly of functional protein structures in species from yeasts to mammals.
See: Yeast and cancer cells – common principles in lipid metabolism
See also: Signaling from the Cell Surface to the Genome: Pheromone Response in the Sexually Aroused
Yeast Cell . . . . . . . . . . . . . . . . . . . . . . . . . . . . .21 Evolution: A View from the 21st Century
Excerpt:

The two-stage replication proofreading system in E. coli and other bacteria has more complex analogues in nucleated eukaryotic organisms, from yeast to plants and animals.2

Excerpt:

There are two particularly significant facts about the S. cerevisiae mating pheromone response:

• It provides a concrete example of how one cell can communicate through well-defined molecular events with the genome of another cell. This example shows that we cannot consider the genome in any way isolated from the outside world; it is a fully informed cell organelle that works dynamically in response to a wide range of organic and inorganic inputs.

• The yeast pheromone response system utilizes sophisticated and complex sensory and signaling components (such as a G protein-coupled receptor) that researchers have encountered repeatedly in many quite distant organisms [160].

Proof-reading is nutrient energy-dependent and pheromone-controlled in species from microbes to humans. The ab initio creation of energy is linked from the de novo creation of G protein-coupled receptors and cell type differentiation via energy-depnedent chemotaxis and phototaxis. Both are required to find food and to remember where to find it. Nutrient selection is the link to energy-dependent translation of codon identify from the paternal lineage, which involves different cell types. Cell type differentiation is nutrient-dependent and pheromone-controlled in species from microbes to humans.
See also: Learning from Bacteria about Natural Information Processing
See for contrast: 7/25/13
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.

In some species that sexually reproduce, one of the sexually-differentiated cell types is called a spermatozoa. The other is called the ovum. In both energy-dependent sexually-differentiated cell types RNA interference is essential for cellular quiescence. The quiescence links autophagy to the transgenerational epigenetically-effected stability of organized genomes in all cell types.
In our 1996 Hormones and Behavior review, we put RNA-mediated interference (RNAi) into the context of sexual differentiation of cell types via the pheromone-controlled energy-dependent physiology of sexual reproduction.
See: From Fertilization to Adult Sexual Behavior
Abstract excerpt: 

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.”

Unlike Jay R. Feierman, others have since recently decided to continue Addressing sex as a biological variable, which is probably what all serious scientists have always done. It is difficult to imagine why anyone who is not a serious scientist would link mutations and/or natural selection to the evolution of sex differences in cell types.
See:

This themed issue of the Journal of Neuroscience Research highlights sex differences of the brain at all scales, from the genetic and epigenetic, to the synaptic, cellular, and systems differences—differences known to be present throughout the life span.

My comment: Epigenetically-effected sex differences in the brain that develop during the lifespan have been linked from nutrient energy-dependent biophysically constrained RNA-mediated protein folding chemistry to fixation of amino acid substitutions such as VAl158Met, which links energy-dependent behavioral transitions from adolescence to adulthood in humans.
See for example: Oppositional COMT Val158Met effects on resting state functional connectivity in adolescents and adults
The function of the amino acid substitution is altered by a single nucleotide polymorphism (SNP) in COMT (G-to-A base-pair substitution) leading to a methionine (Met) valine (Val) substitution at codons 108/158 (COMT Val158Met). Carriers of the Met allele display a fourfold decrease in enzymatic activity compared to Val allele carriers. The decrease is accompanied by an increase of prefrontal DA activity. (Lachman et al. 1996; Lotta et al. 1995).
See also: Amino acids and virus penetration
Conclusion:

Theorists have ignored what serious scientists have detailed in the context of energy-dependent RNA methylation and cell type differentiation that must link learning and memory from ecological variation to ecological adaptation via the conserved molecular mechanisms of protein folding biochemistry that link metabolic networks to genetic networks.  The amount of ignorance is overwhelming, and the theorists are not attempting to inform themselves.

Even Tim Bredy’s group seems to have fallen behind after publication of Experience-Dependent Accumulation of N6-Methyladenosine in the Prefrontal Cortex Is Associated with Memory Processes in Mice

They clearly linked energy-dependent RNA-methylation from learning and memory to RNA-mediated cell type quiescence and to sex differences in cell types in species from yeasts to mammals. With publication of Genetic and epigenetic factors underlying sex differences in the regulation of gene expression in the brain, they appear to ignore their prior claims, which link learning and memory in spermatozoa to the ability to find the ovum, which is another biophysically constrained sexually differentiated cell type. That energy-dependent ability of a sperm cell to find an ovum becomes increasingly important in the context of other published works such as this one. Mitochondrial genome and epigenome: two sides of the same coin

That claim made me more interested in seeing what I could find by scanning the table of contents in the Journal of Neuroscience Research :An Issue Whose Time Has Come: Sex/Gender Influences on Nervous System Function

From what initially saw, no one is addressing the facts about how energy-dependent biophysically constrained protein folding chemistry links RNA-mediated amino acid substitutions to supercoiled DNA via the physiology of pheromone-controlled reproduction in species from marine microbes to humans. Perhaps the special issue only claims to be Addressing Sex as a Biological Variable — 20 years after we did that.

See for comparison: From Fertilization to Adult Sexual Behavior (1996)

Excerpt:

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.”

See also: Misunderstanding cancer
The fact that detection of accumulated mutations does not provide diagnostic clarity should eliminate theories about accumulated mutations and evolution. How could mutations not be linked to physiopathology, but somehow lead to the evolution of biodiversity. For example, see the conclusion from Mutation-Driven Evolution: “…genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world. In this view of evolution there is no need of considering teleological elements” (p. 199).
I cited several different works from Tim Bredy’s group and am grateful to him for helping to inform me after I asked him about microRNAs in November 2012. All works from Tim Bredy’s group and the works of others can now be placed into the context of this one: Single-nucleotide polymorphism rs948854 in human galanin gene and multiple sclerosis: a gender-specific risk factor

These data demonstrate for the first time an association between rs948854 polymorphism and multiple sclerosis and, further, that this association is sex specific.

Why isn’t someone else linking the energy-dependent change in the base pair to changes in hydrogen-atom tranfer in DNA base pairs in solution in all living genera and linking the changes in base pairs to amino acid substitutions that determine thei differences in all cell types? It’s not just about sex differences and never has been. All cell type differentiation is energy-dependent and all biodiversity is controlled by the physiology of reproduction.

Before you read anything else from the special issue Journal of Neuroscience Research: An Issue Whose Time Has Come: Sex/Gender Influences on Nervous System Function, I recommend that you read Genetic and epigenetic factors underlying sex differences in the regulation of gene expression in the brain

How else are they going to link cell type differentiation in species from microbes to humans via sex differences without including what was known about genetics and molecular epigenetics 20 years ago? No matter how hard they try to ignore the facts we presented in the molecular epigenetics section of our 1996 review and all other facts about energy-dependent cell type differentiation, they cannot escape the fact cell type differentiation is energy-dependent and controlled by the physiology of reproduction.
I’ll let you know more about what I find in other articles from the same special issue when I have time to unravel any attempts to obfuscate facts that serious scientists have always know, like this one: Feedback loops link odor and pheromone signaling with reproduction
See Energy-dependent maternal-to-zygotic transition (in prep)

Physics

Life is energy-dependent task management

See also: Life is energy-dependent task management (2)
Press Release: The Nobel Prize in Chemistry 2016 

for the design and synthesis of molecular machines

Excerpt:

They have developed molecules with controllable movements, which can perform a task when energy is added.

My comment: When energy is added is the key to understanding healthy longevity in the context of popular information
Popular information (link opens pdf)
Excerpt:

All chemical systems strive for equilibrium – a lower energy state – but this is somewhat of a stalemate. We can take life as an example. When we eat, the body’s molecules extract the energy from the food and push our molecular systems away from equilibrium, to higher energy levels. The biomolecules then use the energy to drive the chemical reactions necessary for the body to work. If the body was in chemical equilibrium, we’d be dead.
Just like the molecules of life, Sauvage’s, Stoddart’s and Feringa’s artificial molecular sytems perform a controlled task. Chemistry has thus taken the first steps into a new world.

My comment: All steps that were designed to link energy as information to the physiology of reproduction and healthy longevity existed at the dawn of creation.  Chemistry finally links the differences between Old Earth Creationists (OEC) and Young Earth Creationists (YEC). The OEC appear to have assumed that the reaction times Schrodinger (1944) placed into the context of his claims in “What is Life?” occur across billions of years.
Excerpt:

Indeed, in the case of higher animals we know the kind of orderliness they feed upon well enough, viz. the extremely well-ordered state of matter in more or less complicated organic compounds, which serve them as foodstuffs. After utilizing it they return it in a very much degraded form -not entirely degraded, however, for plants can still make use of it. (These, of course, have their most power supply of ‘negative entropy’ the sunlight.)

In that context the emergence of energy automagically linked the “Big Bang” to theories about all reaction times. The reaction times linked what organisms eat to natural selection for mutations. Theorists may still think that de Vries 1902 definition of ‘mutation’ links their assumptions to the evolution of all biodiversity.
In 1991, Roger Penrose succinctly addressed that problem with the theorists claims in the forward to the reprint edition of “What is Life?

How often do we still hear that quantum effects can have little relevance in the study of biology, or even that we eat food in order to gain energy?

My comment: The answer to that question was placed into the context of “…his discoveries of mechanisms for autophagy,” when Yoshinori Ohsumi won the 2016 Nobel Prize in Physiology or Medicine.
Virus-driven energy theft is the link to all negative outcomes in the context of autophagy. The nutrient-dependent pheromone-controlled physiology of reproduction in species from microbes to mammals is the link from RNA-mediated protein folding chemistry to all biophysically constrained limits on life.
Life exemplifies natural selection for codon optimality, which links RNA-mediated amino acid substitutions to supercoiled DNA, which protects all organized genomes from virus-driven entropy.  The virus-driven theft of quantised energy links changes in base pairs to amino acid substitutions in viruses that facilitate their energy dependent replication. Differences in their rate of replication can be compared to differences in rates of energy-dependent cell type differentiation and proliferation in all cell types of all individuals of all living genera.
That has already been done in the context of the Precision Medicine Initiative and National Microbiome Initiative, which link energy-dependent differences in metabolic networks to genetic networks via the pheromone-controlled physiology of reproduction in species from microbes to humans.  If the fine-tuned balance of life in all its diversity is not maintained by the proper use of available energy, nutrient-stress and/or social stress link energy-dependent viral latency to all pathology.
See: Epigenetics and Genetics of Viral Latency

… viral latency is responsible for life-long pathogenesis and mortality risk…

My comment: When the 2017 Nobel Prizes in the hard sciences are again awarded to those who are Combating Evolution to Fight Disease, which is what happened in 2015, how many more times will neo-Darwinian theorists and “Big Bang” cosmologists try to dumb-down the findings on how energy as information biophysically constrains cellular differentiation and proliferation in the context of ecological variation and energy-dependent ecological adaptations?

terrarium-eco-system

Theorists can't understand biology

See also: Neuroplasticity
Thanks to Teresa Binstock for calling my attention to this:
 

Biology is imposssible

Optimizing neuroplasticity by linking atoms to ecosystems

Thanks to Anna Di Cosmo for calling the attention of others to this:

My comment: Attempts to explain the “binding problem” of integration in the context of ecoimmunology and disease ecology compared to emergence and evolution are examples of how much pseudoscientific nonsense has been accepted and touted in the context of the neo-Darwinian “Modern Synthesis.” For comparison, serious scientists have detailed a model of top-down causation that links the design of the brain from the bottom up in an atoms to ecosystems model of cell type differentiation. The model links our experiences from our first breath to our behavior during life history transitions via biophysically constrained protein folding.
Re: “Man is the measure of all things.” Intelligent scientists understand that their measurements from physics, chemistry, and the molecular mechanisms of biologically-based cause and effect must link all other scientific disciplines to biology.
See for example: Oxygen regulation of breathing through an olfactory receptor activated by lactate
Conclusion:

Although ORs [olfactory receptors] were first identified for their role in smell, they may be involved in myriad chemosensory pathways detecting endogenous and exogenous ligands throughout the body.

For comparison to what is known to serious scientists about receptor-mediated cause and effect in the context of chemosensory pathways, evolutionary theorists and theoretical physicists continue to misrepresent all measures of all things. For example, they refuse to explain how “re-evolution” of the bacterial flagellum occurred in four days but claim that an example of no evolution in ~2 billion years supports the claims included in the “Modern Synthesis.”
See: Scientists discover organism that hasn’t evolved in more than 2 billion years
See: Evolutionary resurrection of flagellar motility via rewiring of the nitrogen regulation system
My comment: Try to place the evolutionary resurrection of flagellar motility into the context of the binding problem that must link receptor-mediated events to chemosensory pathways after watching this video.

The bacteria that “re-evolved” their flagella over a weekend exemplify how the nutrient-dependent pheromone-controlled physiology of reproduction links ecological variation to ecological adaptation in all living genera via receptor-mediated events that link food odors and pheromones to the physiology of reproduction in all living genera.
For comparison, Simon LeVay challenged my model of ecological adaptation, which resolved issues of the “binding problem” that links receptor-mediated behaviors in the context of sex differences in cell types and differences in sexual orientation.
See: Gay, Straight, and the Reason Why: The Science of Sexual Orientation
Excerpts:

That the odor of gay men is recognizably different from the odor of other people is believable, although the claim hasn’t been independently verified and its chemical basis hasn’t been studied. (p. 209)
It seems unlikely to me, though, that gay men have an innate preference for the odor of gay men over that of straight men because many gay men are attracted to straight men and, given the opportunity, will have sex with them even in preference to gay partners. Thus this finding, if replicable, is more likely to represent a learned association resulting from gay men’s prior history of intimacy with other gay men. (p. 210)
James Kohl, an independent researcher who also markets “human pheromones” to the general public, believes that pheromones may have a primary influence in setting up a person’s basic sexual orientation. Other, more consciously perceived aspects of attractiveness, such as facial appearance, are attached to a person’s basic orientation through a process of association during early postnatal life, according to Kohl. 35 (p. 210)
This model is attractive in that it solves the “binding problem” of sexual attraction. By that I mean the problem of why all the different features of men or women (visual appearance and feel of face, body, and genitals; voice quality, smell; personality and behavior, etc.) attract people as a more or less coherent package representing one sex, rather than as an arbitrary collage of male and female characteristics. If all these characteristics come to be attractive because they were experienced in association with a male- or female-specific pheromone, then they will naturally go together even in the absence of complex genetically coded instructions. (p. 210)
Still, even in fruit flies, other sensory input besides pheromones — acoustic, tactile, and visual stimuli — play a role in sexual attraction, and sex specific responses to these stimuli appear to be innate rather than learned by association [36.]. We simply don’t know where the boundary between prespecified attraction and learned association lie in our own species, nor do we have compelling evidence for the primacy of one sense over another. (p. 210 – 211)

The chapter 8 notes entry number 36 attempts to show there is “…no compelling evidence for the primacy of one sense over another.” LeVay tries to support that ridiculous claim by citing Spieth (1974) “Courtship behavior in Drosophilia” and Stockinger et al (2005) “Neural circuitry that governs Drosophilia male courtship
Excerpt:

Anatomical differences in this circuit that might account for the dramatic differences in male and female sexual behavior are not apparent.

My comment: In our 1996 Hormones and Beahavior review, From Fertilization to Adult Sexual Behavior, we placed anatomical differences and sex differences in behavior into the context of RNA-mediated cell type differention. The conserved molecular mechanisms we detailed in our section on molecular epigenetics extend across species, regardless of whether LeVay or anyone else can find sex differences in neuroanatomy that correlate with differences in the behaviors of flies and humans.
See for comparison: Courtship behavior in Drosophila melanogaster: towards a ‘courtship connectome’

Excerpt: 

The construction of a comprehensive structural, and importantly functional map of the network of elements and connections forming the brain represents the Holy Grail for research groups working in disparate disciplines.

My comment: None of my former colleagues from the Society for the Scientific Study of Sexuality has since made any attempt to challenge LeVay’s claims about my model. However, LeVay’s claims can be compared in the context of two recent reports from serious scientists:
1) Feedback loops link odor and pheromone signaling with reproduction
Excerpt:

Compelling evidence that links the feedback loops from microbes to humans

2) MicroRNA-encoded behavior in Drosophila
Conclusion:

The results of this study contribute to the understanding of how complex innate behaviors are represented in the genetic program. Our data lead us to propose that other miRNAs might also be involved in the control of behavior in Drosophila and other species.

See also: The protein arginine methyltransferase PRMT5 promotes D2-like dopamine receptor signaling, which was reported as: Receptor methylation controls behavior 
Excerpt:

Likhite et al. found putative arginine methylation motifs in some human G protein–coupled receptors (GPCRs), including the D2 dopamine receptor, and in homologs in the worm Caenorhabditis elegans.

My comment: Nutrient-dependent RNA-directed DNA methylation of GPCRs in nematodes and humans, links the pheromone-controlled physiology of reproduction to the nutrient-dependent pheromone-controlled physiology of reproduction in yeasts and other microbes via the conserved molecular mechanisms of cell type differentiation we detailed in our 1996 review. Serious scientists have linked the facts from our review from the epigenetic landscape to the physical landscape of DNA in the organized genomes of all living genera.
See: DNA twist as a transcriptional sensor for environmental changes (1992) and DNA supercoiling and bacterial gene expression (2006) and Flagellar and global gene regulation in Helicobacter pylori modulated by changes in DNA supercoiling (2007).
Addendum: Only pseudoscientists and other who are among the biologically uninformed have failed to accept the scientific progress that led to publication of Structural diversity of supercoiled DNA (2015).
This parody links what is known to serious scientists about biologically-based cause and effect to the ridiculous claims of theorists in an amusing musical rendition of insults to the theorists that is unlike any other collection of polite insults that you may ever see.

See also: Combating Evolution to Fight Disease
My comment: Help serious scientists to force pseudoscientists to learn about biologically-based cause and effect. Join the fight to stop the pseudoscience and preventable diseases!

Compare what is known to serious scientist to the claims of these pseudoscientists in the context of the most recent attempt to convince others that evolution is true.

Evolution website sets out to tackle great scientific unknowns

Excerpt: 

The site was created by a team led by Simon Conway Morris, Professor of Evolutionary Palaeobiology and a Fellow of St John’s College at the University of Cambridge. “Evolution is true, and if it didn’t happen, we wouldn’t be here,” he said.

My comment: Are you willing to accept that circular logic rather than examine life in the context of Schrodinger’s claims from “What is Life?
Excerpt:

Indeed, in the case of higher animals we know the kind of orderliness they feed upon well enough, viz. the extremely well-ordered state of matter in more or less complicated organic compounds, which serve them as foodstuffs. After utilizing it they return it in a very much degraded form -not entirely degraded, however, for plants can still make use of it. (These, of course, have their most power supply of ‘negative entropy’ the sunlight)

My comment: The anti-entropic epigenetic effect of the sun’s virucidal energy on DNA repair links ecological variation to nutrient-dependent ecological adaptation via the physiology of reproduction or to virus-driven pathology in all living genera. That is not circular logic, and molecular mechanisms linked to the physiology of nutrient-dependent reproduction exemplify how the differences between life and death arose.
See also: Consciousness Mechanics: The Movie for more philosophical nonsense than most people have seen integrated into something to entertain the masses.
 

terrarium-eco-system

Cell type differentiation: atoms to ecosystems

Relaxed genetic control of cortical organization in human brains compared with chimpanzees

Abstract conclusion:

A major result of increased plasticity is that the development of neural circuits that underlie behavior is shaped by the environmental, social, and cultural context more intensively in humans than in other primate species, thus providing an anatomical basis for behavioral and cognitive evolution.

Reported as:

Nature and nurture: Human brains evolved to be more responsive to environmental influences

Excerpt:

…the morphology of the human cerebral cortex is substantially less genetically heritable than in chimpanzees and therefore is more responsive to molding by environmental influences.

They claim ecological variation is linked to ecological adaptations, but link nature and nurture to evolution. Serious scientists report that the epigenetic landscape leads to more flexible changes in the physical landscape of our DNA compared to the DNA of other primates. Cognition does not evolve. Pseudoscientists cannot seem to grasp the fact that one amino acid substitution is the reference point for the differences between chimpanzees and modern humans compared to gorillas. See my posts to the Neuroscience FB group on this topic.   I am no longer allowed to comment to the phys.org news site because this report and many other recent reports continue to contradict earlier reports on cell type differentiation and Chimpanzee intelligence Chimpanzee intelligence determined by genes
See also: Nothing in Biology Makes Any Sense Except in the Light of Evolution
Excerpt:

…the so-called alpha chains of hemoglobin have identical sequences of amino acids in man and the chimpanzee, but they differ in a single amino acid (out of 141) in the gorilla. ( p. 127)

See also: From Fertilization to Adult Sexual Behavior
Excerpt:

This discourse calls attention to features that are central to the so-called nature-nurture discussion.

My comment: See our section on molecular epigenetics. It is ridiculous to continue pretending that RNA-mediated amino acid cell type differentiation can be placed into the context of “evolution.” Nature and nurture are linked by RNA-mediated gene duplication and by RNA-mediated amino acid substitutions, not by mutations and evolution. The systems complexity exemplified in different cell types links the sun’s biological energy from atoms to ecosystems. Cell type differentiation is nutrient energy-dependent and controlled by the physiology of reproduction.  Viruses steal the energy that cells need to differentiate and that organisms need to reproduce. When the accumulation of viruses links the proliferation of viral microRNAs to pathology it is because cells do not have the unlimited power to adapt to ecological variation. Simply put, without proper nutrition, virus-driven stress causes all pathology in all cell types of all individuals of all living genera.

For example: The major antigenic changes of the influenza virus are primarily caused by a single amino acid near the receptor binding site.
My comment: Viruses kill individuals and cause the extinction of species via single amino acid substitutions. If you cannot understand how that fact is linked to the fact that …the so-called alpha chains of hemoglobin have identical sequences of amino acids in man and the chimpanzee, but they differ in a single amino acid (out of 141) in the gorilla. ( p. 127) you are not likely to ever become a biologically informed serious scientist.
See also: Ten Craziest Things Cells Do

Viruses perturb the biophysically constrained RNA-mediated protein folding chemistry that typically enables the differentiation of cell types that links atoms to ecosystems and all differences in morphological phenotypes and all differences in behavioral phenotypes — none of which “evolve.”
 

terrarium-eco-system

Conserved molecular mechanisms

Functional Conservation of the Glide/Gcm Regulatory Network Controlling Glia, Hemocyte and Tendon Cell Differentiation in Drosophila
Abstract excerpt:

High throughput screens allow us to understand how transcription factors trigger developmental processes including cell specification. A major challenge is the identification of their binding sites because feedback loops and homeostatic interactions may mask the direct impact of those factors in transcriptome analyses.

My comment: Evolutionary theorists must accept the fact that feedback loops and homeostatic interactions are conserved and stop making ridiculous claims about mutations and evolution. Virus-driven genomic entropy is not something that can be conserved across species via natural selection. Only a biologically uninformed science idiot would dare to suggest such a thing, or to keep suggesting it more than a decade after serious scientists have detailed the links from the microRNA/messenger RNA balance to cell type differentiation in all living genera.