See also: A two-faced protein enables RNA-mediated DNA repair (3)

The importance of DNA repair to heritability cannot be understated. Theorists who think in terms of mutations and evolution are biologically uninformed and may never have learned anything about DNA repair. Serious scientists are overloaded with information and are not likely to try to explain facts about biologically based cause and effect to theorists.

November, 2015 An individual-based diploid model predicts limited conditions under which stochastic gene expression becomes advantageous

My comment: Stochastic Gene Expression (SGE)-modifier genes is another term that theorists may use to confuse anyone who is close to understanding how cell type differentiation occurs in the context of thenutrient-dependent microRNA/messenger RNA balance. Theorists keep trying to explain missing heritability in the context of diseases and the beneficial mutations that they have linked to evolution via natural selection. They have no facts to use, so they use correlations.

July, 2015 Haplotypes of common SNPs can explain missing heritability of complex diseases

My comment: The haplotypes are correlates that have little explanatory power to serious scientists.

November 2015 Loss of Ezh2 promotes a midbrain-to-forebrain identity switch by direct gene derepression and Wnt-dependent regulation

Excerpt: The change of brain area identities caused by loss of Ezh2 involves H3K27me3-mediated derepression of forebrain-specific transcription factors and indirect reduction of canonical Wnt signaling due to derepression of Wnt signal inhibitors. Thus, our study identifies epigenetic repression of multiple transcription factors and a central signaling pathway as a key mechanism in sustaining brain growth and regional identity.

My comment: The molecular mechanisms of epigentically effected RNA-mediated cell type differentiation are perfectly clear in species from microbes to man. They have been consistently linked from protein biosynthesis and degradation to healthy longevity or from virus perturbed protein folding and mutations to aging and pathology.

September 2015 Protein biogenesis machinery is a driver of replicative aging in yeast

Excerpt:

Directly targeting certain failing protein complexes or downstream deleterious effects results in replicative lifespan extension, but we suggest that many of these effects will prove to be cell type- and growth condition-specific. Our model predicts that a more robust extension of lifespan may be possible in many organisms by targeting the causal factor in aging, protein biogenesis. Indeed, altering the rates of protein production (i.e. translation) or degradation (i.e. autophagy) have repeatedly been shown to influence longevity across a wide range of organisms (see (Wasko and Kaeberlein, 2014; Johnson et al., 2013; Cuervo, 2008).

My comment: Despite the number of reports that now link the microRNA/messenger RNA balance to healthy longevity or to disease, theorists have not grasped the facts about RNA-mediated cell type differentiation.

November 2015 MicroRNA mechanisms of action: what have we learned from mice?

Conclusion:

We speculate that miRNAs emerged during evolution to increase the complexity of gene regulation, thereby contributing to the diversity of organisms.

My comment: These theorists place everything known to serious scientists about how nutrient-dependent microRNAs link ecological variation from atoms to ecosystems via transgeneral epigenetic effects on RNA-mediated cell type differentiation in all living genera into the context of emergence and the evolution of biodiversity.

For comparison, a search for “microRNA” yields more than 45,000 published papers indexed at PubMed. How did their review of the extant literature lead them to such a tragic conclusion about how different cell types are created and how they change during life history transitions by as little as a single amino acid substitutions?

All speculation about the emergence of microRNAs and links to the evolution of increasing organismal complexity manifested in biodiversity is based on pseudoscientific nonsense. More than 45,000 journal articles attest to that fact. Arguable the ~42,000 journal articles that mention evolution might enable appropriate comparisons, if the mention of evolution was accompanied by facts about how it occurs. Serious scientists have learned how to link ecological variation to ecological adaptations in mice and all living genera. And this is what we have learned about humans from mice.

Nutrient-dependent/pheromone-controlled adaptive evolution: a model June 14, 2013

Excerpt:

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.

My comment: The fact that no other model links ecological variation to ecological adaption in all living genera seems to mean nothing to neo-Darwinian theorists. It is obvious that they will continue to frame their ridiculous ideas about biologically-based cause and effect in the context of emergence and the evolution of increasing organismal complexity manifested in biodiversity.

For example:

…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).  — Mutation-Driven Evolution June 14, 2013

My comment: When placed into the context of my model, the textbook claim about mutation-driven evolution is the most ridiculous claim any theorist could make. It makes no sense in the context of what is known to serious scientists about microRNAs and RNA-mediated cell type differentiation.

June 2014 Regulation of histone methylation by noncoding RNAs

Excerpt 1)

In all organisms the stable inheritance of phenotypic states is achieved by a combination of genetic and epigenetic means [1]–[3]. Precise DNA replication and chromosome segregation mechanisms transmit a complete blueprint of genes from parental to progeny cells through mitotic and meiotic cell divisions [4]–[6]. The accuracy of this process is of paramount importance for survival.

Excerpt 2)

2) Unlike genetic alterations, epigenetic changes occur in the absence of mutations to the underlying genes.

My comment: The epigenetic changes link the epigenetic landscape to the physical landscape of supercoiled DNA via histone methylation and other RNA-mediated epigenetic effects in species from microbes to humans.

For example, see: CryoEM and computer simulations reveal a novel kinase conformational switch in bacterial chemotaxis signaling

It was reported as: Researchers resolve structure of a key component of bacterial decision-making

Excerpt:

A new study offers atomic-level details of the molecular machinery that allows swimming bacteria to sense their environment and change direction when needed.

My comment: The nutrient-dependent pheromone-controlled links from atoms to ecosystems were established in the context of the report on re-evolution of the bacterial flagellum that occurred in 4 days. The fact that this was placed into the context of atomic-level resolve extends the atoms to ecosystems perspective to all structures and functions in all cell types of all individuals of all living genera.

Conclusion:

To know how this mechanical system works, we need to know the structure,” he said. “Once we open the clock, see how the gears fit together, then we can start thinking about how the clock actually works. The gears of the bacterial brain are now in place.

My comment: The “gears” of the “brain” are linked to the “gears” of the “re-evolved” bacterial flagellum in 4 days by 2 nutrient-dependent amino acid substitutions in another microbial species. That suggests the molecular mechanisms may be the same in all individuals of all living genera, unless there is a different model that links ecological variation from atoms to ecosystems and ecological speciation and all morphological and behavioral biodiversity. Let’s compare what is currently known about ecosystems and ecological speciation to the evidence of evolution that is still touted by biologically uninformed evolutionary theorists.

The Blind Watchmaker: Why the Evidence of Evolution Reveals a Universe without Design

Description:

Twenty years after its original publication, The Blind Watchmaker, framed with a new introduction by the author, is as prescient and timely a book as ever. The watchmaker belongs to the eighteenth-century theologian William Paley, who argued that just as a watch is too complicated and functional to have sprung into existence by accident, so too must all living things, with their far greater complexity, be purposefully designed. Charles Darwin’s brilliant discovery challenged the creationist arguments; but only Richard Dawkins could have written this elegant riposte. Natural selection―the unconscious, automatic, blind, yet essentially nonrandom process Darwin discovered―has no purpose in mind. If it can be said to play the role of a watchmaker in nature, it is the blind watchmaker in nature.

My comment: Richard Dawkins is not a scientist. The claim that his book has ever been prescient or timely is ridiculous.

See for comparison: From Fertilization to Adult Sexual Behavior

Nineteen years after publication of our Hormones and Behavior review of RNA-mediated sex differences in cell types, the nutrient-dependent pheromone-controlled physiology of reproduction has linked our section on molecular epigenetics from atoms to ecosystems in the context of microRNAs and cell adhesion proteins that protect supercoiled DNA from virus-driven genomic entropy.

The pheromone-controlled protection arises in the context of what is currently known to all serious scientists about RNA-mediated links to all cell type differentiation in all individuals of all living genera. Everything known about RNA-mediated cell type differentiation eliminates the ridiculous portrayals of evolution by Richard Dawkins and other biologically uniformed science idiots.

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