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in attempts to explain any aspect of species-specific biophysically constrained cell type differentiation and aging has been replaced by the use of model systems of biological processes.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.

 

Biology to a Physicist

Abiogenesis vs microRNA biogenesis

Summary: The pseudoscientific nonsense about abiogenesis that has been touted by Karo Michaelian and others like him has caused the unnecessary suffering and premature death of millions to billions of people by placing the pathogenic consequences of deregulated miRNAs into the context of ridiculous theories.
See for comparison: Structural diversity of supercoiled DNA and the parody from the same research group:
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Abiogenesis (2017)
Microscopic dissipative structuring and proliferation at the origin of life (Oct 13, 2017)

Some fundamental molecules of life are suggested to have been formed, proliferated, and evolved through photochemical microscopic dissipative structuring and autocatalytic proliferation under the UV-C/UV-B solar environment prevalent at Earth’s surface throughout the Archean. Evidence is given in the numerous salient characteristics of these, including their strong absorption in this spectral region and their rapid non-radiative excited state decay through inherent conical intersections. The examples of the dissipative structuring and dissipative proliferation of the purines and of single strand DNA are given. UV-C and UV-B-induced stationary state isomerizations and tautomerizations are shown to be crucial to the formation of the purines from hydrogen cyanide in an aqueous environment under UV-C light, while UV-C induced phosphorylation of nucleosides and denaturing of double helix RNA and DNA are similarly important to the production and proliferation of single strand DNA. This thermodynamic dissipation perspective provides a physical-chemical foundation for understanding the origin and evolution of life.

The suggestion is ridiculous. No serious scientist would claim that some fundamental molecules of life formed, proliferated, and evolved in the context of thermodynamic dissipation after the UV-C induced phosphorylation of nucleosides and denaturing of double helix RNA and DNA.
The functional structure of supercoiled DNA is energy-dependent.
All serious scientists start with the link from the sun’s anti-entropic virucidal energy on contact with water to the creation of ATP synthase; the creation of microRNAs; the creation of all other enzymes; the creation of all receptors; the creation of all hormones. That’s how serious scientists link microRNA biogenesis to all biophysically constrained food energy-dependent pheromone-controlled morphological and behavioral diversity on Earth.
MicroRNA biogenesis (2018)

The tipping point of 72,000 indexed published works that mention microRNAs was reached on 4/18/18
See: microRNA
Example: Arthropod viruses and small RNAs (2013)

Understanding the role of small RNAs in arthropod host-virus molecular interactions will facilitate manipulation of these pathways for both management of arthropod pests of agricultural and medical importance, and for protection of beneficial arthropods such as honey bees and shrimp. This review highlights recent research on the role of small RNAs in arthropod host-virus interactions with reference to other host-pathogen systems.

Example: MicroRNAs as mediators of insect host-pathogen interactions and immunity (2014)

In this review, we will discuss the latest developments in regards to the role of microRNA in insect host-pathogen interactions and provide some insights into this rapidly developing area of research.

Example: miRNA regulation of innate immunity (2018)

MicroRNAs (miRNAs) are small noncoding RNA and are pivotal posttranscriptional regulators of both innate and adaptive immunity. They act by regulating the expression of multiple immune genes, thus, are the important elements to the complex immune regulatory network. Deregulated expression of specific miRNAs can lead to potential autoimmunity, immune tolerance, hyper-inflammatory phenotype, and cancer initiation and progression. In this review, we discuss the contributory pathways and mechanisms by which several miRNAs influence the development of innate immunity and fine-tune immune response. Moreover, we discuss the consequence of deregulated miRNAs and their pathogenic implications.

The pseudoscientific nonsense touted by Karo Michaelian and others like him has caused the unnecessary suffering and premature death of millions to billions of people by placing the pathogenic consequences of deregulated miRNAs into the context of ridiculous theories.
See for comparison: Structural diversity of supercoiled DNA and the parody from the same research group:

See also: Michaelian K
and Retraction: Oligoarginine peptides slow strand annealing and assist non-enzymatic RNA replication (Nov 23, 2017)
The life’s works of all those who have ever touted their ridiculous claims about abiogenesis can now be placed into the context of the eternal significance of microRNAs. The energy dependent de novo creation of microRNA flanking sequences has repeatedly been linked from the physiology of pheromone-controlled reproduction to biophysically constrained viral latency and sympatric speciation in all living genera.
See: Dependence of RNA synthesis in isolated thymus nuclei on glycolysis, oxidative carbohydrate catabolism and a type of “oxidative phosphorylation” (1964)

The synthesis of RNA in isolated thymus nuclei is ATP dependent.

See also: Long-range coherence and energy storage in biological systems (1968)
See also: Cytosis (for ages 10+)

Players take turns placing workers on available organelles within a human cell in order to collect resources (such as Carbohydrates or ATP!) or take actions (such as purchasing Cell Component cards or translating mRNA into Proteins!)

Players use their resources to build Enzymes, Hormones, and Hormone Receptors and also to help detoxify the cell – all of which score health points. The player with the most health points at the end of the game wins!

See for comparison: DNA Denaturing through UV-C Photon Dissipation: A Possible Route to Archean Non-enzymatic Replication (2014)

Many of the fundamental molecules of life, those common to all three domains; bacteria, eukaryote, and archea, including RNA and DNA, amino acids, enzymes, vitamins, cofactors, and protoporphyrins, absorb photons in the UV-C 1. RNA or DNA in complexes with these molecules act as acceptor quenchers, providing the electronically excited pigment donor molecule with an extremely rapid (sub picosecond) non-radiative dexcitation channel, through internal conversion into vibrational energy of the nucleic acid and surrounding water molecules2.

On January 15, 2016 John Hewitt commented:  You have just described the founding principle and thermodynamic function of life
On April 17, 2018, I commented on the ridiculous claim this so-called science journalist made because he blocked me from seeing his tweets a few months ago.

God's shrinking role in salvation (2)

Conclusion: There is no such thing as a blind dance of atoms. Quantized energy-dependent changes link angstroms to ecosystems in all living genera via the physiology of reproduction. Serious scientists do not link “high-level cause and purposes” to anything that does not link what organisms eat from food energy to the physiology of reproduction. Only pseudoscientists claim that ideas about “emergence” are “…a remarkable synthesis across fields and levels.”
See: God’s shrinking role in salvation

These 6 Common Vegetables Are Actually All The Same Plant Species
The morphological traits are quantized energy-dependent, They link the de novo creation of plant microRNAs from the anti-entropic virucidal energy of sunlight to the physiology of reproduction in all living genera via the energy-dependent creation of microRNAs in animals.
See: Viral MicroRNAs, Host MicroRNAs Regulating Viruses, and Bacterial MicroRNA-Like RNAs

The interactions of these small noncoding RNAs in such primitive species have wide-reaching effects, from increasing viral and bacterial proliferation, better responses to stress, increased virulence, to manipulation of host immune responses to provide a more ideal environment for these pathogens to thrive. Here, we explore those roles to obtain a better grasp of just how complicated disease truly is.

Disease is much more complicated when it cannot be linked from top-down causation via physics, chemistry, and molecular biology. See for comparison; ‘Liquid Light’ Can Bend Around Objects in a Frictionless Flow
Thanks to Fiona Myrglwitz for calling attention to this claim that they can:

…conceive and design future photonic superfluid-based devices where losses are completely suppressed.

That suggests they may link the metabolism of bacteria from the creation of uranium isotopes to the errors made in mathematical models of evolved traits. The errors in mathematical models fail to link quantized energy-dependent changes in the microRNA/messenger RNA balance to the biophysically constrained by the physiology of reproduction.The errors are magnified by the fact that they fail to link incompletely suppressed energy losses to all pathology via the virus-driven degradation of messenger RNA.

For comparison, the physiology of reproduction links the solar analemma to the biophysically constrained energy in uranium, which is the reason that radiation therapy is used to treat cancer. Everything known about the link from sunlight to radiation therapy can be placed into context via use of the Mobius strip.
It is an example of how nutrient energy-dependent pheromone-controlled choices made by all living genera must link feedback loops to the biophysically constrained virucidal energy of sunlight. Any loss of energy can potentially be linked to the proliferation of viruses via a slight drop in the potential of hydrogen (pH).

That fact makes it more be obvious that God’s shrinking role in salvation can be viewed in the context of medical practices that appear to make physicians and/or other medical professionals your savior(s). They will warn you to avoid too much sun exposure and treat your cancer with radiation because you did not get enough sun exposure to protect you via the increased production of Vitamin D.
They will tell you to use a chemical “sun-screen” and treat your cancer with chemotherapy that was caused by the chemical imbalance your body could no longer cope with.
See also: Electrolytes induce long-range orientational order and free energy changes in the H-bond network of bulk water
This was reported as: A single ion impacts a million water molecules
So far as I know there has been no discussion of the link from free energy changes in the H-bond network to the hydrophobicity of supercoiled DNA, which links quantum physics to the protection of all organized genomes from the virus-driven degradation of messenger RNA and genomic entropy.
Could the lack of discussion be attributed to the claim that no one understands quantum mechanics in an age where the speed of light on contact with water has been linked to all biodiversity via energy-dependent changes in angstroms to ecosystems in all living genera?
From last year: How Can Physics Underlie the Mind? Top-Down Causation in the Human Context

My review on Amazon (6/12/16)

Others linked the sun’s anti-entropic virucidal energy from energy-dependent changes in hydrogen-atom transfer in DNA base pairs in solution to supercoiled DNA, which protects all organized genomes from virus-driven energy theft and genomic entropy.

Ellis comments on at least one of Schrodinger’s claims from “What is Life?” but he largely ignores the energy-dependent links from ecological variation to ecological adaptation that also were reported in two recent publications. See: “Structural diversity of supercoiled DNA” and “Epigenetics and Genetics of Viral Latency.”

Ellis cannot be held accountable for not knowing the most recent work (May 11, 2016) reported that “…viral latency is responsible for life-long pathogenesis and mortality risk…”

However, it seems inappropriate for anyone whose opinions are held in high regard to ignore everything else that is known about energy-dependent RNA methylation and the biophysically constrained morphological and behavioral diversity of all living genera. Experimental evidence has established facts that are being used to link the Precision Medicine Initiative to the National Microbiome Initiative via attempts to crack the olfactory code.

When researchers report the direct link from energy-dependent RNA methylation to differences in behavior, this book will be compared to Masatoshi Nei’s “Mutation-driven evolution.” The biggest difference between the two seems to be that Ellis tries to link emergence to evolution via Darwin’s “conditions of life.”

But he now bears the burden of the report in “Science” of nutrient energy-dependent pheromone-controlled weekend evolution of the bacterial flagellum: “Evolutionary resurrection of flagellar motility via rewiring of the nitrogen regulation system.”

The “resurrection” is obviously energy-dependent and it also links the innate immune system to biophysically constrained biologically-based cause and effect in species from microbes to humans via RNA-mediated amino acid substitutions. Resurrecting Darwin’s “conditions of life” after they were ignored by neo-Darwinists for many decades should not be attempted by physicists, cosmologists, or biologically uninformed theorists from any other discipline without first learning more about what is known about the RNA-mediated links from physics and chemistry to molecular epigenetics.

See for comparison, this review by

An admirable, systematic approach to the issue of emergence from physics to sociology, of great originality, broad scope, and deep understanding. George Ellis argues with admirable clarity of thought that much of the world we live in is governed not by the blind dance of atoms, but by high-level causes and purposes. This is a much needed book and a remarkable synthesis across fields and levels. I know of no other book where the evidence for emergence is presented so thoroughly and with as much insight.

There is no such thing as a blind dance of atoms. Quantized energy-dependent changes link angstroms to ecosystems in all living genera via the physiology of reproduction. Serious scientists do not link “high-level cause and purposes” to anything that does not link what organisms eat from food energy to the physiology of reproduction. Only pseudoscientists claim that ideas about “emergence” are “…a remarkable synthesis across fields and levels.”

See: God’s shrinking role in salvation (3)
IMG_3010

Base pairs, amino acids and phenotypes

Holliday junction trap shows how cells use recombination and a junction-guardian role of RecQ helicase

DNA repair by homologous recombination (HR) underpins cell survival and fuels genome instability, cancer, and evolution.

Autophagy is the established link from energy-dependent changes in base pairs and RNA-mediated amino acid substitutions to DNA repair in the context of polycombic ecological adaptations that prevent the hecatombic evolution of virus-driven pathology. Inventing new detailed models of DNA repair serves only to confuse those who have already linked energy-dependent changes from angstroms to ecosystems via the physiology of reproduction, which links the innate immune system to supercoiled DNA and all biodiversity in all living genera.
See for comparison. This is another confusing attempt to link energy-dependent autophagy via the physiology of pheromone-controlled reproduction from changes is base pairs to RNA-mediated amino acid substitutions, which differentiate all cell types in all living genera in the context of polycombic ecological adaptations.
Very few published works use the term RNA regulons for comparison to energy-dependent changes in microRNAs in the context of hydrogen-atom transfer in DNA base pairs in solution. The changes in base pairs must be linked to the post-transcriptional events via biophysically constrained RNA-mediated protein folding chemistry, which links metabolic networks to genetic networks in all living genera.
RNA regulons: coordination of post-transcriptional events (2007)

Here I describe several recently discovered examples of RNA operons in budding yeast, fruitfly and mammalian cells, and their potential importance in processes such as immune response, oxidative metabolism, stress response, circadian rhythms and disease. I close by considering the evolutionary wiring and rewiring of these combinatorial post-transcriptional gene-expression networks.

The claims about RNA regulons in the context of the innate immune system and claims about a model of biologically-based cause and effect were included in this model.
See: Nutrient-dependent/pheromone-controlled adaptive evolution: a model. My model is a refutation of the neo-Darwinian nonsense about beneficial mutations, natural selection and evolution. Natural selection for energy-dependent codon optimaility links the pheromone-controlled physiology of nutrient-dependent reproduction to all biodiversity in all living genera via polycombic ecological adaptations.
The refutation of neo-Darwinian nonsense is supported by experimental evidence from many different published works that link energy-dependent changes in base pairs to fixation of RNA-mediated amino acid substitutions in organized genomes. The ~55,000 indexed published works on nutrient energy-dependent microRNAs and virus-driven energy theft can now be place into these claims about the hecatombic evolution of all virus-driven pathology
See:Freeze-frame’ proteins show how cancer evolves: Researchers capture elusive clues about cells’ path to cancer.

“The intermediate molecules are the most important parts of biochemical reactions,” said Rosenberg… “They define what the reaction is and how it will proceed. But because they are transient and elusive, it’s really difficult to study them, especially in living cells.

The “intermediate molecules” are energy-dependent microRNAs. They link hydrogen-atom transfer in DNA base pairs in solution to all cell type differentiation in all genera via microRNA flanking sequences.
See: The phylogenetic utility and functional constraint of microRNA flanking sequences

Both miRNAs and their flanking sequences provide phylogenetic signals suitable for the inference of phylogeny with high levels of accuracy, when sufficient numbers of this type are concatenated. As detailed here, the clear identity and easy alignment of these sequences makes them good candidates for estimating phylogeny, and they can reliably be found and identified across all members of a clade of interest. Their relatively slow evolution [3] also means that they can easily be identified in de novo assemblies of genomes.

There is no such thing as the de novo assemblies of genomes or relatively fast or slow evolution. Cell type differentiation is energy-dependent and biophysically constrained. Energy-dependent changes in the microRNA/messenger RNA balance are required to link the epigenetic landscape to the physical landscape of supercoiled DNA.
Everything known about energy-dependent biophysically constrained RNA-mediated protein folding chemistry was placed into the context of Combating Evolution to Fight Disease.  Simply put, the innate immune system defends all cell types against the virus-driven evolution of cancer and all other pathology.

As predicted in “The Darwin Code,” That fact has forced A radical revision of human genetics

“…geneticists don’t have an accurate understanding of how mutations behave in people who are not obviously sick. “This is a fascinating flashpoint in the field right now,” says Robert Green, a geneticist at Brigham and Women’s Hospital in Boston, Massachusetts. “Many people are deeply concerned that widespread screening of ostensibly healthy people could actually lead to harm.”

The harm comes from not knowing how nutrient energy-dependent RNA-mediated cell type differentiation occurs. The availabiity of nutrients varied in the ancestors of people from Asian, African, Latino and other non-European ancestries. That is why…

…failing to include people from Asian, African, Latino and other non-European ancestries is holding back understanding of how genes influence disease by limiting the view of human genetic diversity.

Natural selection of food for energy-dependent codon optimality links base pairs and amino acid substitutions to sex specific cell type differences and all other RNA-mediated cell type differences.

See for example: Gender-Specific Association of Galanin Polymorphisms with HPA-Axis Dysregulation, Symptom Severity, and Antidepressant Treatment Response (2010)

Human galanin (GAL) is a 30 amino-acid neuropeptide, proteolytically processed from preprogalanin (PPGAL) (Evans and Shine, 1991; Schmidt et al, 1991). PPGAL is a single-copy gene located on chromosome 11q13.3–13.5, spanning over 6 kb of genomic DNA and organized into six exons (Rokaeus and Brownstein, 1986; Vrontakis et al, 1987).

Single-nucleotide polymorphism rs948854 in human galanin gene and multiple sclerosis: a gender-specific risk factor (2017)

Although it remains to be demonstrated whether A-to-G substitution in rs948854 leads to an increased or decreased transcriptional activity of the GAL gene, functional studies suggest a decrease of galanin level in the minor G allele carriers. It has been shown that reduction in galanin level leads to or exacerbates neurodegeneration, whereas an increased galanin level has neuroprotective effects (Hobson et al., 2008; Elliott-Hunt et al., 2011; Liu et al., 2013). Furthermore, galanin may exhibit anti-inflammatory effects, possibly via inhibition of excitatory neurotransmitter release and/or regulation of cytokine production by activated microglia (Hokfelt et al., 1987; Su et al., 2003; Elliott-Hunt et al., 2004). The associations between rs948854 variants and MS demonstrated in the current study support our hypothesis that polymorphism in the promoter region that are likely to change expression level of the GAL gene affect the cause and the outcome of MS, shifting the balance in favor of either neuroprotection or neurodegeneration.

Modeling Recent Human Evolution in Mice by Expression of a Selected EDAR Variant (2013)

Alternatively, it could be precisely the pleiotropic nature of 370A that allowed multiple distinct selective forces to act on this variant over its long history, when many of the postulated selective pressures such as temperature and humidity changed dramatically. The fact that EDAR acts mostly on ectodermal appendages and that the phenotypic effects of the 370A allele are not extreme reduces the costs of pleiotropy and would facilitate this process. Thus, what were initially neutral changes in some appendages driven by 370A would gain adaptive significance in the face of new selective pressures. It is worth noting that largely invisible structural changes resulting from the 370A allele that might confer functional advantage, such as increased eccrine gland number, are directly linked to visually obvious traits such as hair phenotypes and breast size. This creates conditions in which biases in mate preference could rapidly evolve and reinforce more direct competitive advantages. Consequently, the cumulative selective force acting over time on diverse traits caused by a single pleiotropic mutation could have driven the rise and spread of 370A.

My comment: 370 A exemplifies an energy-dependent change in rs3827760, which is also known as 1540T/C, 370A or Val370Ala. It is a single nucleotide polymorphism (SNP) linked from a base pair change to an amino acid substitution in the ectodysplasin A receptor EDAR gene on chromosome 2.
A genome-wide analysis of putative functional and exonic variation associated with extremely high intelligence (2015)

One SNP rs4713668 (P=4.62 × 10−4) identified in our study, was in LD (r2=0.65) with rs3227, which is one of the three variants recently reported with genome-wide significant evidence of association with educational attainment.46

A genetic basis of variation in eccrine sweat gland and hair follicle density (2015)
rs3827760 appears to have become En1 [Engrailed-1), and modulation of En1 levels became a driver of natural differences in eccrine gland and hair follicle density between mouse strains. Previously, those differences were linked to a single energy-dependent base pair change and one amino acid substitution.

This finding not only provides insight into a distinct molecular program that promotes increased eccrine gland density, but also reveals that this effect on eccrine development occurs at the expense of hair follicles in a tissue where the two appendage types are naturally interspersed.

The link to behavior via visually obvious traits such as hair phenotypes and breast size is missing. That means there is no link to sex differences and biases in mate preference via rs948854. That means everything known to serious scientists about biophysically constrained RNA-mediated amino acid substitutions and cell type differentiation in all individuals in all living genera may continue to be ignored.
See for instance: Nutrient-dependent/pheromone-controlled adaptive evolution: a model

Two additional recent reports link substitution of the amino acid alanine for the amino acid valine (Grossman et al., 2013) to nutrient-dependent pheromone-controlled adaptive evolution. The alanine substitution for valine does not appear to be under any selection pressure in mice. The cause-and-effect relationship was established in mice by comparing the effects of the alanine, which is under selection pressure in humans, via its substitution for valine in mice (Kamberov et al., 2013).

These two reports (Grossman et al., 2013; Kamberov et al., 2013) tell a new short story of adaptive evolution. The story begins with what was probably a nutrient-dependent variant allele that arose in central China approximately 30,000 years ago. The effect of the allele is adaptive and it is manifested in the context of an effect on sweat, skin, hair, and teeth. In other mammals, like the mouse, the effect on sweat, skin, hair, and teeth is due to an epigenetic effect of nutrients on hormones responsible for the tweaking of immense gene networks that metabolize nutrients to pheromones. The pheromones control the nutrient-dependent hormone-dependent organization and activation of reproductive sexual behavior in mammals such as mice and humans, but also in invertebrates as previously indicated. That means the adaptive evolution of the human population, which is detailed in these two reports, is also likely to be nutrient-dependent and pheromone-controlled, since there is no other model for that.

The fact that there is no other model of energy-dependent biophysically constrained cell type differentiation that also links virus-driven energy theft to all pathology has not escaped the attention of those who might wish they had a model. Because they don’t, all they can do is claim that no model refutes their ridiculous theories about evolution.

For a failed discussion attempt of everything known to serious scientists about energy-dependent base pair changes, RNA-mediated amino acid substitutions and cell type differentiation, see Creationism May 22, 2016

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This open access article may be too technical for most people to discuss, but Creationism is difficult to discuss outside the context of energy-dependent creation compared to energy theft and pathology.

A genome-wide association scan implicates DCHS2, RUNX2, GLI3, PAX1 and EDAR in human facial variation

My summary of the excerpt: They linked an energy-dependent changes in rs3827760 from the base pair to the same amino acid substitution, which had already been linked to cell type differentiation across populations of modern humans. Fixation of the energy-dependent base pair change in the amino acid substitution that differentiates the morphological and behavioral phenotypes of modern humans links supercoiled DNA to protection from virus-driven energy theft and genomic entropy in species from archaea to all primates.
In the same study they linked virus-driven energy theft to loss of function mutations and transgenerational epigenetic inheritance of healthy longevity for comparison to mutation-driven pathology via the mouse model. The mouse to human model was already used to link the EDAR variant to similar morphological differences in humans. The morphological differences appear to link the Zika virus pathology to craniofacial changes and differences in brain development via what is known about the bull sperm microRNAome and presence of microRNAs in human breast milk that protect infants from virus-driven energy theft during the first few years of development.
Excerpt:

The derived G allele at the index SNP in this region (rs3827760) encodes a functional substitution in the intracellular death domain of EDAR (370A) and is associated with reduced chin protrusion (Table 2). EDAR is part of the EDA signalling pathway (comprising EDA, EDAR and EDARADD (the EDAR-binding death domain adaptor protein)) which specifies prenatally the location, size and shape of ectodermal appendages (such as hair follicles, teeth and glands)23. The death domain has been shown to be involved in the interaction of EDAR with EDARADD, the 370A form having higher activity than the ancestral variant24. The G allele at rs3827760 is not present in Europeans and Africans but is seen at high frequency in East Asians and is essentially fixed in Native Americans (Table 3). This SNP has been associated in East Asians with characteristic tooth morphologies, hair type and sweat gland density25, 26, 27. Recently, we showed, in the same study sample examined here, that rs3827760 impacts on aspects of pinna morphology, including: lobe size and attachment, ear protrusion and helix rolling12. Mutations in the EDA pathway cause hypohidrotic ectodermal dysplasia28. This disorder is characterized by a reduced number of sweat glands, oligodontia, decrease in the amount of hair and facial dysmorphia, including a markedly protrusive chin29.”

Energy-dependent base pair changes are the only known link from RNA-mediated amino acid substitutions to cell type differentiation via supercoiled DNA and protection from virus-driven energy theft. The energy-dependent base pair changes prevent the entropy of organized genomes.
The focus of my 2013 model was on the RNA-mediated amino acid substitutions that differentiate all cell types in all individuals of all living genera. The focus of theorists has been to obfuscate what is known about the links from energy-dependent base pair changes to RNA-mediated amino acid substitutions and cell type differentiation, which is the only way to explain biologically-based cause and effect. It also explains why some species survived and others became extinct during the past ~6000 years.
See for example:
Analysis of 6,515 exomes reveals the recent origin of most human protein-coding variants
Genome divergence and diversification within a geographic mosaic of coevolution
Difference in Plumage Color Used in Species Recognition between Incipient Species Is Linked to a Single Amino Acid Substitution in the Melanocortin-1 Receptor
Substitutions Near the Receptor Binding Site Determine Major Antigenic Change During Influenza Virus Evolution
Identification of amino acid substitutions supporting antigenic change of influenza A(H1N1)pdm09 viruses.
The fact that all divergence and diversification in all living genera must be energy-dependent and the fact that virus-driven energy theft causes all pathology must be ignored by those whose financial support for their research comes from the evolution industry or the big bang cosmology industry. We cannot expect much scientific progress until the financial constraints are broken and the biophysical constraints on energy-dependent RNA-mediated cell type differentiation are addressed at every level from angstroms top ecosystems after starting from quantized energy-dependent changes in base pairs.
See for comparison: Lineage-Specific Genome Architecture Links Enhancers and Non-coding Disease Variants to Target Gene Promoters
Re: “…the interactomes of 31,253 annotated promoters in 17 human primary blood cell types.”
Excerpt:

Here, we link thousands of GWAS SNPs to their putative target genes and prioritize more than 2,500 potential disease-associated genes, three-quarters of which were not previously implicated.

Reported as: Researchers identify missing links that connect human DNA variation with disease
All “missing links” are nutrient energy-dependent and biophysically constrained by the physiology of reproduction. They link RNA-mediated amino acid substitutions to cell type differentiation in all cell types of all living genera via the innate immune system and supercoiled DNA. Mathematical models are useless in that context. They are based on inferences and assumptions.
It’s time to finish this blog post. I linked energy-dependent changes in SNPs from amino acid substitutions to cell type differentiation via a model of biologically-based cause and effect, and the “science” news is still reporting biologically-based cause and effect in the context of their pseudoscientific nonsense about mathematical models of inferences and assumptions.

rp_levels-of-organization.jpg

Biophotonics, glycobiology, quantized biodiversity (2)

From Fertilization to Adult Sexual Behavior (1996)
In our section on Molecular epigenetics, we wrote:

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.

My comment: Serious scientists have since learned that all cell type differences arise from alternative splicings of otherwise identical genes. Pseudoscientists still make claims about the emergence of life and link natural selection to structural biology and the function of genome organization.

See for comparison: A Big Bang in spliceosome structural biology (2016)

Excerpt:

Splicing cycles through a series of steps in which the spliceosome assembles on the intron-containing pre-mRNA, defining the boundaries between exons—the sequences ultimately retained in the mature mRNA—and introns (see the figure, panel A).

My comment: Energy-dependent changes in angstroms to ecosystems link the defined boundaries between exons and introns from ecological variation to ecological adaptation and all biodiversity.  The “Big Bang” in structural biology is a contextualized polite way to tell theoretical physicists and other theorists that energy-dependent changes in functional structures must link ecological variation to ecological adaptation via what is known to serious scientists about all the links from angstroms to ecosystems in all living genera. Others have been trying to tell theorists how to link biologically-based cause and effect for several years.

See for example (2007): The MicroRNA miR-124 Promotes Neuronal Differentiation by Triggering Brain-Specific Alternative Pre-mRNA Splicing
Excerpt:

Both microRNAs and alternative pre-mRNA splicing have been implicated in the development of the nervous system (NS), but functional interactions between these two pathways are poorly understood.

My comment: All serious scientists know that the functional interactions among microRNAs and alternative pre-mRNA splicing are nutrient energy-dependent and controlled by the physiology of reproduction. Do you know how energy-dependent RNA methylation links biophysically constrained protein folding chemistry to cell type differentiation via RNA-mediated amino acid substitutions? If not, you probably do not know why  information about amino acid substitutions was left out of the claim that linked chromatin to the control of behavior in this misrepresentation:
Chromatin controls behavior
Conclusion:

…the discoveries of Yang et al. are an important addition to an emerging literature implying a dynamic epigenome in the central nervous system (14, 15), which is contrary to the prevailing dogma in the epigenetics field.

My comment: There is no prevailing dogma in the epigenetics field. The dogma was eliminated when serious scientists linked energy-dependent changes from angstroms to ecosystems via epigenetic effects of sensory input on the innate immune system; the de novo creation of G protein-coupled receptors; the physiology of reproduction, and fixation of RNA-mediated amino acid substitutions that link supercoiled DNA to protection from virus-driven energy theft and genomic entropy in all organized genomes of all living genera.
See also: Chromatin remodeling inactivates activity genes and regulates neural coding.
Summary: Epigenetic regulation in the brain

The activity of neurons in the brain controls the transcription of genes that influence the pruning of dendritic connections between neurons, and such modifications can influence animal behavior. Yang et al. propose a role for chromatin remodeling by the nucleosome remodeling and deacetylase complex (NuRD) in the inactivation of such activity-dependent transcription in the mouse cerebellum (see the Perspective by Sweatt). Deposition of the histone variant H2A.z at promoters of activity-dependent genes required the NuRD complex. Loss of the NuRD complex function resulted in hypersensitivity of mice to sensory stimuli and excessive neuronal connectivity in animals performing a task on a treadmill.

This article was reported as: Ability to turn off genes in brain crucial for learning, memory
Excerpt (with my emphasis):

One process that controls chromatin structure and transcription is chromatin remodeling by energy-dependent protein complexes (4). Such complexes that depend on adenosine 5′-triphosphate (ATP) can control gene expression by moving, ejecting, or restructuring nucleosomes, the scaffolds around which DNA wraps. Each nucleosome contains a core particle of eight histone protein subunits (5). Remodeling events include posttranslational modifications, swapping individual One process that controls chromatin structure and transcription is chromatin remodeling by energy-dependent protein complexes (4). Such complexes that depend on adenosine 5′-triphosphate (ATP) can control gene expression by moving, ejecting, or restructuring nucleosomes, the scaffolds around which DNA wraps. Each nucleosome contains a core particle of eight histone protein subunits (5). Remodeling events include posttranslational modifications, swapping individual histone subunit isoforms into and out of the core particle, and facilitating the unbinding of DNA from the core particle.
into and out of the core particle, and facilitating the unbinding of DNA from the core particle.

My comment: Chromatin remodeling is energy-dependent. But, they buried the facts about how energy-dependent chromatin remodeling links sensory input from learning and memory to fixation of RNA-mediated amino acid substitutions. The substitutions differentiate all cell types of all individuals of all living genera, which explains why they invented the term histone subunit isoforms.
Serious scientists understand why pseudoscientists bury facts by stringing words together without telling others what a histone subunit isoform is, or what differentiates one histone subunit isoform from any other histone subunit isoform. In this case, the wordplay prevents others from learning that the availability of nutrients and nutrient energy-dependent changes links link fixation of RNA-mediated amino acid substitutions from learning and memory to chromatin remodeling and the control of behavior. Pseudoscientists tend to remove facts from consideration and remove the facts from the context of via well established pathways that link the epigenetic landscape to the physical landscape of supercoiled DNA  in all living genera.
See for example: Roles of Mutation and Selection in Speciation: From Hugo de Vries to the Modern Genomic Era
Excerpt:

…we will not consider geographical and ecological factors because of space limitation. Our primary purpose is to clarify the roles of mutation and selection in the evolution of reproductive isolation and show that the molecular basis of speciation is more complicated than generally thought at present. (p. 813)

My comment: Inventing the term histone subunit isoform outside the context of geographical and ecological factors is another way to dismiss the complexity of speciation.
See for example: This article mentions a subunit isoform in the context of Loss of the V-ATPase B1 Subunit Isoform Expressed in Non-Neuronal Cells of the Mouse Olfactory Epithelium Impairs Olfactory Function
Excerpt:

The present study is the first to indicate the relevance of the VATPase, and presumably of V-ATPase-mediated proton secretion, in olfactory function. Undoubtedly, further functional and behavioral studies will allow a more comprehensive assessment of the physiological and clinical significance of V-ATPase expression in sustentacular and microvillar cells of the olfactory epithelium. At this point, we can only speculate on such possibilities. For example, modulating olfactory H+ secretion could offer the ability of up- or down-regulating the threshold of detection for certain odorants. Moreover, since the NML plays a role as a barrier against inhaled pathogens, and microbial and chemical toxins, regulating mucus pH may be relevant for protection against various specific diseases.

My comment: If you are unable to link the modulation of olfactory H+ secretion from hydrogen-atom transfer in DNA base pairs in solution to the de novo creation of G protein-coupled receptors and all energy-dependent biodiversity via RNA-mediated amino acid substitutions, please see:
Every amino acid matters: essential contributions of histone variants to mammalian development and disease.
Excerpt:

The introduction of these minor sequence variants into chromatin is physiologically relevant and fundamental to eukaryotic cellular plasticity. However, with the exception of substitutions towards modification permissive amino acids (for example, both H3.1A31 and H3.2A31 to H3.3S31, which can be phosphorylated), it remains unclear how histone variants acquire and/or differentially enrich for specific chemical modifications that are distinct from their canonical counterparts.

My comment: They just muddied the perfectly clear waters of how phosphorylation and fixation of RNA-mediated amino substitutions is links from biophysically constrained protein folding chemistry to all biodiversity via hydrogen-atom transfer in DNA base pairs in solution.   The claim that “every amino acid matters” is placed into the context of what is not known about biophysically constrained protein folding chemistry and biologically-based cause and effect. That is a way to help ensure these researcher get more funding. It’s a common tactic. If you focus on what is not known, people will think it’s not known to serious scientists who are funded to produce results that are supported by their experimental evidence of biologically-based cause and effect.

See also my comment on RNA and dynamic nuclear organization

Excerpt:

Moving forward, if RNA-mediated events organize the cell nucleus, mutations manifested in perturbed protein folding are not likely to lead to natural selection and the evolution of biodiversity. The requirement for DNA to be found in organized genomes is biophysically constrained via the conserved molecular mechanisms of protein biosynthesis and degradation in species from microbes to man.

For simplicity, see:

See also: Structural diversity of supercoiled DNA and m1A and m1G disrupt A-RNA structure through the intrinsic instability of Hoogsteen base pairs, which was reported as:

DNA’s dynamic nature makes it well-suited to serve as the blueprint of life.

My comment: The claim that DNA is the blueprint of life resurrects long-dead gene-centric theories. I expected others to make more rapid progress after the Zechiedrich lab linked energy-dependent changes from angstroms to ecosystems, but Al-Hashimi’s group is still reporting links in the context of pseudoscientific nonsense linked to neo-Darwinian theory. The theory does not address the need for biophysically constrained RNA-mediated protein folding chemistry in the context of the physiology of reproduction.
Perhaps Al-Hashimi’s group will be next to do that in RNA Structural Modules Control the Rate and Pathway of RNA Folding and Assembly, which supposedly is “In Press.” RNA methylation is clearly the link to all biodiversity. But, until then, they may fall behind even further, especially if they keep trying to placate the neo-Darwinists.
See: ‘Quantum jitters’ could form basis of evolution, cancer
Excerpt:

“This is a remarkable study that illuminates a fundamental mechanism responsible for the random mutations that drive evolution and contribute to cancer,” said Bert Vogelstein, M.D., a cancer researcher at Johns Hopkins University School of Medicine who was not involved in this research.

My comment: How did Vogelstein arrive at his ridiculous conclusion? Did Visualizing transient Watson-Crick-like mispairs in DNA and RNA duplexes inadvertently or deliberately lead him to it?
Excerpt:

These results, together with previous structural studies showing that WB and WC-like mispairs can exist within polymerase1–3 and ribosome5,6,13 active sites, strongly suggest that energetic competition between WB and WC-like mispairs is robust and is a key determinant of misincorporation probability during replication and translation (Supplementary Discussion 9).

My comment: How difficult would it have been to clarify the issues involved that suggest energetic competition causes the mutations, which means they do not randomly occur? I reiterate: Vogelstein thinks the “…study illuminates a fundamental mechanism responsible for the random mutations that drive evolution and contribute to cancer…”
Despite everything known to serious scientists about energetic competition for nutrients, I’m sure Vogelstein is not the only biologically uninformed cancer researcher who believes in neo-Darwinian theory. Others may also think that results framed in the context of energetic competition support ridiculous theories. Unfortunately, most people are not going to fight their way through an article like this one to discover that Vogelstein and all others like him are wrong.
Early myeloid lineage choice is not initiated by random PU.1 to GATA1 protein ratios
Excerpt:

These observed protein dynamics are incompatible with random and cross-regulatory PU.1–GATA1 co-expression acting as the central mechanism that initiates MegE versus GM lineage choice3.

My comment: Most people may miss the fact that they claimed “…observed protein dynamics are incompatible with random… co-expression, which initiates lineage choice. Simply put, they eliminated Vogelstein’s ridiculous idea about random mutations from any further consideration.
See also: A miR-155–Peli1–c-Rel pathway controls the generation and function of T follicular helper cells, which was reported as A potential new way to sway the immune system found
Excerpt:

“People know miRNAs are involved in immune response, but they don’t know which miRNAs and how exactly,” explained TSRI Research Associate Zhe Huang, study co-first author with Liu and Seung Goo Kang of TSRI and Kangwon National University.

See also: Regulation of B-cell development and tolerance by different members of the miR-17~92 family microRNAs
Excerpt:

In this experimental setting, the changes in the ratio of virus-transduced CD45.2+ cells (GFP+) versus WT competitors (CD45.1+) during the pro- to pre-B transition provided a measurement for the developmental defect. In the control WT:WT mix group, as no major difference existed between these two populations, the GFP+/CD45.1+ ratios remained unchanged during the pro- to pre-B transition, resulting in a pre-B/pro-B ratio close to 1 (Fig. 5b upper panels and Fig. 5c). In contrast, cells derived from the Mb1tKO HSCs, when transduced with control virus, underwent a severe developmental block in competition with WT cells. Therefore, the GFP+/CD45.1+ ratio shifted drastically as WT cells became dominant in the pre-B population, resulting in a pre-B/pro-B ratio below 0.2 (Fig. 5b middle panels and Fig. 5c).

My comment: All serious scientists know that nutrient energy-dependent microRNA flanking sequences link the innate immune system to differences in morphological and behavioral phenotypes via the physiology of reproduction in species from microbes to man via supercoiled DNA, which protects organized genomes of all living genera from virus-driven entropy.
Recent reports, which link specific families of miRNAs to healthy longevity or to pathology will obviously lead mroe researchers to discover the specific miRNAs that link virus-driven energy theft to all pathology.
See: The phylogenetic utility and functional constraint of microRNA flanking sequences and Role of olfaction in Octopus vulgaris reproduction
Excerpt:

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).

See for comparison: (2016) Codon identity regulates mRNA stability and translation efficiency during the maternal-to-zygotic transition
Excerpt:

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.

My comment: These authors echo the claim that random mutations are not the source of energy-dependent cell type differentiation. They add that the across-species bias of RNA-mediated amino acid substitutions offers an alternative to ridiculous claims about mutation-driven evolution. For another example of facts about RNA-mediated amino acid substitutions, see how Dobzhansky (1973) framed his claims.
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).”

If you don’t like Young Earth Creationists, see also: (2016) Major Evolutionary Blunders: The ‘Degenerate’ Genetic Code?
Excerpts:

A detailed literature review in 2014 found that even if different codons prescribed the same amino acid in a protein, the codon differences still mattered in how the protein was made. The final folding shape of proteins is vital to their function. David D’Onofrio and David Abel documented that the DNA and its corresponding RNA sequence carried information not only for the proper amino acid sequence but also to control the timing of its folding. They “demonstrate that this TP [translational pausing] code is programmed into the supposedly degenerate redundancy of the codon table.”8 What this means is that the code of differing codons, even if they specify the same amino acid, still supplies important information, information that “purposely slows or speeds up the translation-decoding process….Variable translation rates help prescribe functional folding of the nascent protein. Redundancy of the codon to amino acid mapping, therefore, is anything but superfluous or degenerate.”8
…if synonymous codons can have important functional meaning, then the whole methodology goes out the window, and hundreds of studies that used these methods to infer “selection” during the supposed “evolution of genes” could be wrong.11

If you like neo-Darwinian theorists, see: Tempo and mode of genome evolution in a 50,000-generation experiment
Excerpt:

One line of evidence derives from the expectation that synonymous substitutions—point mutations in protein-coding genes that do not affect the amino-acid sequence—are neutral and should therefore accumulate at a rate equal to the underlying mutation rate20,35. This expectation is not strictly true owing to selection on codon usage, RNA folding, and other effects, but…

My comment: Let’s tell the truth with no buts, rather the invent more reasons to lie. Creationists and other serious scientists seem to arrive at the same conclusion by citing different literature that adds another level of epigenetic complexity in the context of non-random selection of RNA-mediated amino acid substitutions, which must be fixed in the organized genomes of all living genera to link the innate immune system to supercoiled DNA, which protects all organized genomes from virus-driven entropy.
The literature includes details about how the across species bias between codons or amino acids and microRNA or pre-mRNAs and mRNA expression levels links selection to efficient, accurate translation, and folding of highly expressed genes.   For comparison, no serious scientist has ever suggested that virus-driven energy theft is linked from mutations and selection to the evolution of one species from another. Thus, it has become perfectly clear that the amount of pseudoscientific nonsense people must believe to continue to believe in mutation-driven evolution is based on definitions and assumptions. Serious scientists do not rely on definitions and assumptions to support their claims.
See for comparison: Mutation-Driven Evolution (2013)

Excerpt:

Mutation is the change of genomic structure and includes nucleotide substitution, insertion/deletion, segmental gene duplication, genomic duplication, changes in gene regulatory systems, transposition of genes, horizontal gene transfer, etc. (2) Natural selection is for saving advantageous mutations and eliminating harmful mutations. Selective advantage of the mutation is determined by the type of DNA change, and therefore natural selection is an evolutionary process initiated by mutation. —

Conclusion:

In other words, 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.

See also: Replace the Modern Synthesis (Neo-Darwinism): An Interview With Denis Noble

[W]hat Haldane, Fisher, Sewell Wright, Hardy, Weinberg et al. did was invent…. The anglophone tradition was taught. I was taught, and so were my contemporaries, and so were the younger scientists. Evolution was defined as “changes in gene frequencies in natural populations.” The accumulation of genetic mutations was touted to be enough to change one species to another…. No, it wasn’t dishonesty. I think it was wish fulfillment and social momentum. Assumptions, made but not verified, were taught as fact.

For more assumptions in the context of ridiculous theories, see: Phylogenetic plasticity in the evolution of molluscan neural circuits (2016)
Conclusion:

Molluscan neural circuitry represents a different evolutionary trajectory from vertebrates and even other lophotrochozoans. Using the same morphogenic genes as other phyla, molluscs have created novel nervous systems that control a wide variety of body forms. Yet the largest brained invertebrates, the cephalopods, have converged with insects and vertebrates on the organization of circuitry for learning and memory. Even with this cross-phyletic convergence, there are intra-phyletic differences between octopus and cuttlefish in the sites of plasticity. Phylogenetic plasticity is also found in gastropods where homologous neurons have been re-used for different functions and where neuromodulatory actions also display species-specificity. One outcome from this work is to show that there are many solutions to the same problem. The story of molluscs is about how looks can be deceiving; the same genes and neurons can be used and reused in different ways to create diverse nervous systems that sometimes converge on the same solution. I think it is more exciting to realize that octopus and mammals independently came up with a learning machine that has a fan-out/fan-in organization and LTP than to think that these similarities are just a family resemblance. Call me a splitter, but I believe that uncovering the many solutions that nature has found will tell us more about fundamental organizational properties than lumping them all together.

My comment: Anyone who makes a ridiculous statement like the one above should be ‘called out’ and questioned to learn how he or she has managed to maintain their overwhelming ignorance despite the availability of publications like this one:
The phylogenetic utility and functional constraint of microRNA flanking sequences and this one The octopus genome and the evolution of cephalopod neural and morphological novelties
Excerpt:

Among the octopus complement of ligand-gated ion channels, we identified a set of atypical nicotinic acetylcholine receptor-like genes, most of which are tandemly arrayed in clusters (Extended Data Fig. 7). These subunits lack several residues identified as necessary for the binding of acetylcholine26, so it is unlikely that they function as acetylcholine receptors. The high level of expression of these divergent subunits within the suckers raises the interesting possibility that they act as sensory receptors, as do some divergent glutamate receptors in other protostomes27. In addition, we identified 74 Aplysia-like and 11 vertebrate-like candidate chemoreceptors among the octopus GPCR superfamily of ~330 genes (Extended Data Fig. 6).

My comment: The GPCR superfamily links receptor-mediated signaling from chemotaxis to phototaxis and all energy-dependent biophysically constrained biodiversity via RNA methylation and RNA-directed DNA methylation, histone acetylation and every aspect of the energy-dependent physiology of reproduction. Taken together, everything known about the energy-dependent receptor-mediated physiology of reproduction links the innate immune system to supercoiled DNA.
Those who tout neo-Darwinian theories for comparison must continue to use definitions and assumptions as if that approach was acceptable to anyone else who was not also a pseudoscientist.
See also: (2016) 33. Octopus Signals
Excerpt:

We define a ‘signal’ as any act or structure which alters the behavior of other organisms, which evolved because of that effect, and which is effective because the receiver’s response has also evolved.

My comment: Via the bastardization of everything known to serious scientists about biologically-based cause and effect, the definition of signal is linked to its evolution via an effect, which is not linked from any epigenetic effect on hormones to any affect on behavior. That makes it impossible to link food odors to the energy-dependent de novo creation of olfactory receptor genes, which are GPCRs. The de novo gene creation of GPCRs links metabolic networks to genetic networks via the pheromone-controlled physiology of behavior in the context of epigenetic effects of pheromones on hormones. The hormones affect the species-specific behaviors of all invertebrates and vertebrates.
Definitions lead to confusion about the use of the terms “effect” and affect, which link epigenetic effects on hormones the the affects of hormones on behavior. Neo-Darwinian theorists skip everything known to serious scientists about the differences between effect and affect and link the definition of a ‘signal’ to species-specific behaviors and all biodiversity.
See for comparison: Feedback loops link odor and pheromone signaling with reproduction

Conclusion:

It appears that GnRH neurons integrate a variety of information about the internal state of the animal and its external environment. At least 10,000 neurons in 26 different brain areas appear to transmit signals directly to GnRH neurons. Among these are areas involved in
odor and pheromone processing, sexual behavior, arousal, reward, and other functions. This suggests that GnRH neurons are poised to modulate reproductive physiology and behavior in accordance with the overall state of the animal.
These studies also indicate that GnRH neurons are likely to influence numerous brain functions. They appear to transmit signals to as many as 30,000 or more neurons in 34 brain areas, consistent with previous studies showing GnRH+ fibers and GnRH receptors in multiple brain regions (Badr and Pelletier, 1987; Jennes et al., 1988; Jennes et al., 1997). BL+ neurons likely to receive synaptic input from GnRH neurons were seen in areas associated with numerous different functions, including odor and pheromone processing, sexual behavior, appetite, defensive behavior, motor programs, and the relay of information to higher cortical areas. These results may reflect a strategy wherein GnRH neurons can modify diverse functions in order to coordinate the internal state of the animal and its behavior with reproduction in order to optimize reproductive success.

My comment: Have neo-Darwinian theorists found a species in which feedback loops do not link what the organism eats to its physiology of reproduction? If not, what do they claim links energy-dependent changes in angstroms to ecosystems in all living genera?
Who cares?

See also: The scent of a hatchling: intra-species variation in the use of chemosensory cues by neonate freshwater turtles

The 5300-year-old Helicobacter pylori genome of the Iceman
Abstract excerpt:

The “Iceman” H. pylori is a nearly pure representative of the bacterial population of Asian origin that existed in Europe before hybridization, suggesting that the African population arrived in Europe within the past few thousand years.

See also: Evolution of gut bacteria in humans and hominids parallels ape evolution
See also: Rapid evolution of microbe-mediated protection against pathogens in a worm host

My comment: Taken  together, these two articles link the difference in the bacteria that nematodes eat to the morphological and behavioral diversity of C. elegans for comparison to the predatory nematode with teeth, P. pacificus. From there, the conserved molecular mechanisms link the gut bacteria of the “Iceman” to the morphological and behavioral diversity of all human populations.

See also:

Special Report on Cell Biology: Sweetening the pot

Glycosylation in cellular mechanisms of health and disease

Glycomics: A rapidly evolving field with a sweet future
Excerpt 1)

Glycans play many critical roles in both the normal function of cells and in disease. They assist in the folding of many proteins, aid in protein trafficking, mediate cell adhesion, differentiate blood groups, modulate the immune system, are implicated in many signaling pathways, and provide a protective extracellular matrix for many types of cells. Glycans are also implicated in the process of infectivity for many pathogenic bacteria (2) and most viruses (3), including those that cause the common cold, influenza, and HIV/AIDS.

Excerpt 2)

Glycomics is now being used in combination with genomics, epigenomics, proteomics, lipidomics and metabolomics to provide a more holistic view of how cellular pathways function and how they change in response to disease.

It has become nearly impossible for me to keep up with the information that refutes neo-Darwinian pseudoscientific nonsense at the same time more articles are published that tout the nonsense.
See for comparison: The role of microRNAs in metabolic interactions between viruses and their hosts
Lineage tracing of human B cells reveals the in vivo landscape of human antibody class switching
Conclusion:

epigenetic inheritance of active and repressed chromatin state during mitosis has been demonstrated (Cavalli and Paro, 1998; Grewal and Klar, 1996). Our measurements suggest that the timescale on which the relative accessibility of IGHC loci persists is ~10 somatic mutations. Calibration of the mutational clock should allow recovery of information about epigenetic state and phenotypic dynamics in units of time and cellular generations. Together with recent studies of mammalian (Spencer et al., 2009) and bacterial cells in culture (Hormoz et al., 2015), our work suggests that phenotypic correlations between sister cells due to shared inheritance are widespread. We predict that such correlations often will be detected when genealogical relationships between individual cells can be resolved. We propose that inheritance of epigenetic state provides a mechanism for orchestrating cellular behavior without the need for signaling.

My comment: Attempts to define the term “signal” will fail because everyone knows what a signal is and all serious scientists know that food odors and pheromones are signals that link feedback loops from the innate immune system to chromatin folding and supercoiled DNA, which protects organized genomes from virus-driven entropy. The proposal the “…inheritance of epigenetic state provides a mechanism for orchestrating cellular behavior without the need for signaling” exemplifies the ignorance of all neo-Darwinian theorists who have failed to link energy-dependent signals to biophysically contrained protein folding chemistry via RNA methylation and RNA-mediated amino acid substitutions that differentiate all cell types in all individuals of all living genera.
Finally,  see:Downstream Antisense Transcription Predicts Genomic Features That Define the Specific Chromatin Environment at Mammalian Promoters
It was reported on August 4, 2016 by Engaging Epigenetic Experts as:

…the authors say that they suspect such antisense transcription plays an important role in “in the regulation of gene expression and the maintenance of a promoter-associated chromatin environment.”

My comment: This site started removing my comments after several weeks of allowing me to accurately link articles like this one to what is known about RNA-mediated cell type differentiation. Others have already invented terms like oncohistones and histone subunit isoforms in attempt to continue obfuscating the links from energy-dependent RNA-mediated amino acid substitutions to healthy longevity because they know virus-driven energy theft has been linked to all pathology.

Engaging Epigenetics Experts appears to be caught in the crossfire. They’ve supported too much neo-Darwinian nonsense to suddenly admit that it never made sense, but that’s what antisense transcription confirms. There are many other sources of what should have been “Science” news but the news was placed into the context of pseudoscientific nonsense touted by neo-Darwinian theorists who have trapped themselves in their ignorance.
In the article mentioned by Engaging Epigenetics Experts, this claim is substantiated:

Despite differences in epigenetic features, tendency for association with transregulatory factors, and capacity to produce stable RNA transcripts, all three classes of TSS described in this work display similarities in sequence content, including enrichment for GC content and Pol II-associated sequence motifs (Fig 2). As such, antisense transcription appears to be encoded in genetic sequence. This connection between sequence content and epigenetic features provides the compelling suggestion that antisense transcription encoded by sequence may direct the positioning of nucleosomes and deposition of histone marks. Antisense transcription may also participate in signal-dependent modulation of epigenetic content where activation of sequence-encoded antisense TSS precedes nearby changes in chromatin structure. In this way, the collection of transcription initiation-associated sequence motifs near promoters may define regulatory potential for a given gene. This connection to sequence also provides a means to interrogate antisense transcription function. Future studies with selective mutation of associated sequence motifs may elucidate the function of antisense transcription and its coincidence with promoter-associated features. Directed mutagenesis could also establish the extent of the effect of antisense transcription on the chromatin environment at promoters.
We characterized downstream antisense transcription initiating near gene promoters in human T47D/A1-2 cells. daTSSs fall between regularly positioned nucleosomes downstream of gene TSSs. Histones within this region are enriched for marks closely associated with active promoter regions, such as H3K4me3 and H3K27ac modifications. Chromatin remodeling complexes show enriched binding upstream of observed daTSS positions, suggesting that antisense transcription contributes to the establishment and maintenance of a promoter-specific chromatin environment. Downstream antisense transcription is common to many human promoters, and daTSSs correlate with the downstream edge of promoter-associated chromatin features. Coincidence of daTSSs with these features suggests interplay between antisense transcription and regulatory pathways.

My comment: There are too many ways to obfuscate what is known about the epigenetically-effected links from energy-dependent changes in angstroms to ecosystems in all living genera. These two paragraphs are important to understand in that context. They link RNA methylation and RNA-mediated amino acid substitutions to cell type differentiation in all living genera via chromatin remodeling, but you will not be encourage to look at the facts because there is no mention of epigenetically-effected RNA-mediated amino acid substitutions in the context of chromatin remodeling.  That’s why I added emphasis to this claim: “…transcription initiation-associated sequence motifs near promoters may define regulatory potential for a given gene.” 
It links hydrogen-atom transfer in DNA base pairs in solution from energy-dependent changes in the microRNA/messenger RNA balance to gene regulation via everything known to serious scientists. It links RNA-mediated amino acid substitutions and morphological diversity by linking energy-dependent RNA methylation from learning and memory to behavior via chromatin remodeling. The chromatin remodeling occurs in the context of the physiology of reproduction and what is known about supercoiled DNA, which protects all organized genomes from virus-driven energy theft and genomic entropy.
But their claim that “…transcription initiation-associated sequence motifs near promoters may define regulatory potential for a given gene” is placed into the context of a theory about the fact that energy-dependent RNA-mediated amino acids substitutions, which are referred to in the context of  transcription initiation-associated sequence motifs may define the energy-dependent regulatory potential of different genes in different individuals of different species. All pseudoscientists know how to obfuscate facts about the energy-dependent regulatory potential of different genes, because they have been placing them into the context of virus-driven energy theft and mutation-driven evolution since the time that de Vries (1902) defined “mutation.”
Addendum: People complain that I am not explaining how quantum physics, quantum chemistry, quantum biology, and quantum consciousness in terms they can understand. See:

Double slit experiment and the REAL secret

Real-world explanation: Brian Greene : What’s Beyond The Double Slit Experiment ?

See also:
 Our Reality Is Information Tom Campbell
Probability & Uncertainty: The quantum mechanical view of nature Richard Feynman
New Experiments Show Consciousness Affects Matter Dean Radin