Serious scientists have known for more than a decade that

…phenotypic variation decreases through geologic time, because microRNAs (miRNAs) increase genic precision, by turning an imprecise number of mRNA transcripts into a more precise number of protein molecules…

See for example: MicroRNAs and metazoan macroevolution: insights into canalization, complexity, and the Cambrian explosion

That fact links the anti-entropic epigenetic effects of nutrient-dependent microRNAs to DNA repair in the organized genomes of species from microbes to man.

Viruses appear to cause the DNA damage via accumulation of viral microRNAs that alters the energy balance of cells and perturb nutrient-dependent protein folding. The time it takes for the balance of DNA damage and DNA repair to cause differences in RNA-mediated gene duplication and the RNA-mediated amino acid substitutions that differentiate cell types has not been established. The range appears to be from ~4 days to longer than ~2 billion years.

The broad range,  was placed into the context of alterations in the energy balance, which were defined by de Vries as mutations. He defined mutations before anything was known about quantum physics, quantum smell, quantum biology or quantum consciousness.

Apparently, population geneticists assumed they could start with de Vries definition and link mutations to evolution via natural selection. Darwin repeatedly claimed the ‘conditions of life’ must be met first. The invention of neo-Darwinism left Darwin’s “conditions” behind. The inventors developed a theory that was based on their assumptions about what mutations could do.

In his 2013 book, Masatoshi Nei decided to try and eliminate natural selection for mutations from the neo-Darwinian theory of evolution. Simply put, selection for beneficial mutations was not a good idea. It was a cart-before-the-horse assumption. Instead, Nei, claimed that evolution had to be due to  “…genomic conservation and constraint-breaking mutation…” because that’s how he assumed it occurred.

See his conclusion in: Mutation-Driven Evolution.

“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” (p. 199).

Teleological elements are considered by others, whether or not they are placed into the context of theology.  A teleology is an account of a given thing’s purpose. For example, a teleological explanation of why forks have prongs is that this design helps humans eat certain foods; stabbing food to help humans eat is what forks are for.

Some theologists appear to think that what they were told to not eat, may be the source of all pathology.  However, like evolutionary theorists, they have been unable to explain how the molecular mechanisms of healthy longevity or pathology evolved.

See, for example: Environmental Epigenetics and a Unified Theory of the Molecular Aspects of Evolution: A Neo-Lamarckian Concept that Facilitates Neo-Darwinian Evolution

Excerpt:

Although the causal role of epimutations was not established in the Darwin’s finch adaptive radiation (Skinner, et al. 2014b) or other models (Brennecke, et al. 2008; Gokhman, et al. 2014; Zeh, et al. 2009), the causal role of genome-wide genetic mutations has also not been established (Laland, et al. 2011).

Their inability to explain anything about the molecular mechanisms of cell type differentiation has led to the invention of terms like epimutations in the context of a neo-Lamarckian theory, which appears to be referred to as a concept to avoid the indication that one theory has simply been added to another.

Thank God, at least a few serious scientists have not accepted Nei’s constraint-breaking mutation “magic”as the ultimate source of all the earth’s biomass. Instead, some scientists have continued to support their claims with experimental evidence of biologically-based cause and effect that links RNA-mediated gene duplication and RNA-mediated amino acid substitutions to cell type differentiation in all living genera.

Indeed, many serious scientists are now aware of at least two things:

1) Glycogen synthase kinase-3 (Gsk-3) plays a fundamental role in maintaining DNA methylation at imprinted loci in mouse embryonic stem cells

Abstract excerpt(s):

Glycogen synthase kinase-3 (Gsk-3) is a key regulator of multiple signal transduction pathways.

Our data demonstrate the importance of Gsk-3 activity in the maintenance of DNA methylation at a majority of the imprinted loci in ESCs and emphasize the importance of Gsk-3–mediated signal transduction in the epigenome.

My comment: Simply put, that means nutrient-dependent metabolic networks must be linked to genetic networks via epigenetically-effected RNA-directed DNA methylation that somehow organizes the genomes of all genera. In other words, all organisms must eat something or they will surely die.

What they eat supplies the amino acids that are required for the formation of proteins. Complex processes of thermodynamic cycles of protein biosynthesis and degradation link the amino acids to cell type differentiation.

For example, see:

2) Glucagon Couples Hepatic Amino Acid Catabolism to mTOR-Dependent Regulation of α-Cell Mass

Reported as: Regulation of Pancreatic Cell Mass

Taken together, those two things explain:

3) Epigenetic silencing of Oct4 by a complex containing SUV39H1 and Oct4 pseudogene lncRNA

Reported as: Pseudogene-derived, long non-coding RNAs (lncRNAs) act as epigenetic regulators of gene expression.

If you look at the extant literature on the de novo creation of olfactory receptor genes and mutations that are linked to the creation of pseudogenes, you may understand the importance of nutrient-dependent RNA-mediated gene duplication and RNA-directed DNA methylation that link RNA-mediated amino acid substitutions to this fact:

FACT: Without evidence for the fixation of the nutrient-dependent RNA-mediated amino acid substitutions in the context of the physiology of reproduction, there would be no experimental evidence that links the epigenetic landscape to the physical landscape of DNA in the organized genomes of all genera.

For contrast, the nutrient-dependent de novo creation of olfactory receptor genes and the epigenetic silencing of olfactory receptor genes appear to link nutrient-dependent microRNAs to repair of damaged DNA that is caused by viruses and the accumulation of viral microRNAs, which perturb protein folding.

FAITH: Viral Genome Junk Is Bunk 

Excerpt:

….viruses likely arose from their hosts and not the other way around. As molecular biologist and biochemist Peter Borger notes, “The most parsimonious answer is: the RNA viruses got their genes from their hosts.”6

Conclusion:  The question is not where the RNA viruses got their genes. In any case, the anti-entropic epigenetic effects of nutrients on RNA-mediated cell type differentiation appear to control viral microRNAs and genomic entropy. The result is increasing organismal complexity in all genera, but not by the evolution of proteins.

That’s why my model starts with the light-induced de novo creation of amino acids. If you learn of a model that links decreases in phenotypic variation across time via the biophysically constrained chemistry of nutrient-dependent RNA-mediated gene duplication and RNA-mediated amino acid substitutions, please tell others about it. They may be willing to compare it to my model of differentiation of the cell types of all genera via fixation of amino acid substitutions in the context of their physiology of reproduction.

Help others explain whatever they think might be the obvious links to a more precise number of protein molecules and differentiated cell types without the magic of evolution. Their faith in science may depend on facts, not theories. If so, they must present the facts, rather than add new theories to old theories and tweak the old theories while doing so.

The theories about beneficial mutations don’t seem to compare well with what is known about RNA-mediated cell type differentiation across generations, which makes it more difficult to accept the extension of any theories across species.

See for instance: How to Make a New Species

The emergence of one species from another occurs… [in the context of ] pheromone mutagenesis [which] might allow researchers to “extend our achievement to other organisms.” (PNAS, 112:4405-10, 2015)

My comment: The honeybee model of nutrient-dependent pheromone-controlled ecological adaptations manifested in morphological and behavioral phenotypes suggests that “emergence” is controlled.

Also see: Vast Complexity of Alternative Splicing in Neurons, which followed from representations made in 2012: Alternative RNA Splicing in Evolution, and in 1996: From Fertilization to Adult Sexual Behavior

Excerpt:

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.

See the discussion of Alternative Splicings on my FB page:

Two more accurate representations of biologically-based cause and effect are:

1) Ancestral diets determine vulnerability to type 2 diabetes

Excerpt:

“Hopefully further research in understanding their gut microbes, which are major producers of Vitamin B12 in our body, and/or dietary supplementation with Vitamin B12 and other micronutrients, could reduce the risk of metabolic diseases in the coming generations,” says Associate Professor Hardikar.

2) Research shows hope for personalized genome sequencing

Excerpt:

…projects like this, which identify the genetic predictors of people who respond to medications vs. people who don’t, are the first steps toward making personalized medicine a reality.

My comment: The honeybee already serves as a model organism for studying human immunity, disease resistance, allergic reaction, circadian rhythms, antibiotic resistance, the development of the brain and behavior, mental health, longevity, diseases of the X chromosome, learning and memory, as well as conditioned responses to sensory stimuli (Kohl, 2012). — Kohl (2013)

The honeybee model organism of life history transitions is linked to personalized medicine by everything currently known about RNA-mediated gene duplication and RNA-mediated amino acid substitutions that differentiate the cell types of all living genera via their physiology of reproduction.

See, for example: Oppositional COMT Val158Met effects on resting state functional connectivity in adolescents and adults

Val158Met is referred to as a genetic variant.  It is a single nucleotide polymorphism (SNP) in the COMT gene that codes catechol-O-Methyltransferase. The polymorphism is a single nucleotide substitution between G–> A. It results in an amino acid change from valine to methionine at codon 158. Theorists link mutations in genes to changes in morphological and behavioral phenotypes  without consideration of the fact that RNA-mediated amino acid substitutions are fixed in the context of the physiology of nutrient-dependent reproduction. If mutations were fixed in species, genomic entropy would invariably lead to their extinction.

Simply put, without RNA-mediated gene duplication and RNA-mediated DNA repair their would be no organisms and no species — except for those that automagically emerged and did not succumb to genomic entropy. Genetic entropy can occur throughout life, although it is typically epigenetically effected by the anti-entropic energy that links nutrient-dependent RNA-mediated gene duplication and cell type differentiation to healthy longevity.  Alternatively, Lead Exposure during Early Human Development and DNA Methylation of Imprinted Gene Regulatory Elements in Adulthood, was reported as Early Lead Exposure Affects Gene Expression Throughout Life 

Excerpt:

“We now have the first human evidence for an association between early lead exposure and three aberrantly methylated regulatory regions of imprinted genes,” says Hoyo. “But from a public health perspective, the results are very exciting because we can begin to think about identifying potential biological markers for early exposure to lead and other toxins in the environment.”

See also: Epigenomic disruption: The effects of early developmental exposures

Abstract excerpt:

Through DNA methylation, histone modifications, and small regulatory RNAs the epigenome systematically controls gene expression during development, both in utero and throughout life. The epigenome is also a very reactive system; its labile nature allows it to sense and respond to environmental perturbations to ensure survival during fetal growth. This pliability can lead to aberrant epigenetic modifications that persist into later life and induce numerous disease states.

My comment: The fact that RNA-mediated events control gene expression throughout life does not seem to be accepted by theorists who appear to believe that mutations in individuals can somehow be linked to the evolution of organisms that must ecologically adapt before they can reproduce.

 

 

 

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