Oliver Sacks: Nature employs conserved molecular mechanisms

May 10, 2014 | James Kohl

The Mental Life of Plants and Worms, Among Others

Oliver Sacks

Oliver Sacks concludes: “Nature has employed at least two very different ways of making a brain—indeed, there are almost as many ways as there are phyla in the animal kingdom. Mind, to varying degrees, has arisen or is embodied in all of these, despite the profound biological gulf that separates them from one other, and us from them.4″

My comment: Conserved molecular mechanisms link the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man via experience-dependent changes that lead to the differentiation of cell types in individuals of different species. Ecological variation results in the ecological adaptations manifested in morphological and behavioral phenotypes.

Oliver Sacks attributes biologically-based cause and effect to ‘Nature” and avoids any mention whatsoever of mutations, natural selection, and evolution. Others would do well to follow his lead, since he has moved across species with examples of nutrient-dependent pheromone-controlled ecological adaptations that eliminate pseudoscientific theories about evolution from any further consideration whatsoever. Clearly, it is sensing and signaling that is required for the ecological, social, neurogenic, and socio-cognitive niche construction that is manifested in increasing organismal complexity. If mutations, natural selection, and evolution were the cause of increasing organismal complexity, Oliver Sacks would probably have mentioned that possibility.

See also:

Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems by James V. Kohl

The Mind’s Eye by Oliver Sacks

The Scent of Eros: Mysteries of Odor in Human Sexuality by James V. Kohl and Robert T. Francoeur

The Mind’s Eyes: Human pheromones, neuroscience, and male sexual preferences by James V. Kohl

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Nutrition, pheromones and cancer (2)

May 10, 2014 | James Kohl

See: Nutrition, pheromones and cancer

Despite the inaccurate reporting of exeperimental evidence, the link from the nutrient-dependent pheromone-controlled microRNA / messenger RNA balance is becoming clearer. Unfortunately, due to the inaccurate reporting, others may need to take the free course: Epigenetic Control of Gene Expression, before they can begin to understand the scientific progress in cancer research, which is occurring because some researchers have dispensed with the pseudoscientific nonsense of evolutionary theory. See for example: Biogenesis of intronic miRNAs located in clusters by independent transcription and alternative splicing

Excerpt: “…alternative splicing might play a role in uncoupling the expression of clustered miRNAs from each other, which otherwise are generally believed to be co-transcribed and co-expressed.”

My comment: Nutrient uptake leads to miRNA biogenesis and alternative splicings that are responsible for the differentiation of cell types. Typically, cell type differentiation leads to controlled growth of cells and to increasing organismal complexity. That fact makes it clear that something must go wrong when cell type differentiation is not controlled.

See for example: Intronic miR-3151 Within BAALC Drives Leukemogenesis by Deregulating the TP53 Pathway

Excerpt: “Whereas intergenic miRs are always regulated by their own promoters, intronic miRs can be either regulated with their host gene or regulated independently of their host gene (28, 29).”

Reported as: Gene within a gene contributes to aggressive leukemia

Excerpt: “…it is high expression of miR-3151 that really matters.”

The microRNA/messenger RNA balance is what really matters because it alters nutrient-dependent cell type differentiation via alternative splicings. When evolutionary theorists learn the cause of normal cell type differentiation, which leads to species diversity, they may stop telling people that mutations and natural selection cause evolution. If not, continuing to tout that nonsense will cause others who know that species diversity is nutrient-dependent and pheromone-controlled to claim that evolutionary theorists have prevented scientific progress towards a cure for cancer.

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Natural Genetic Engineering or Mutation-driven evolution?

May 9, 2014 | James Kohl

Large-Scale Metagenomic-Based Study of Antibiotic Resistance in the Environment

Reported as:

Antibiotic-Resistant Germs, Lying in Wait

by Carl Zimmer 5/8/14

Excerpt: “Their resistance hinted that antibiotic-resistance genes were not just the product of modern medicine, but an ancient part of nature.”

See also:  Horizontal Gene Transfer Regulation in Bacteria as a “Spandrel” of DNA Repair Mechanisms

Excerpt: “DNA uptake control might be linked in part to nutrient requirements [32]. Whether the mechanism associated with DNA uptake defines the fate of the DNA once introduced into the cell is less clear, but the possibility that DNA uptake began as a nutrient uptake mechanism cannot be discounted [32].”

My comment: The nutrient uptake-dependent pheromone-controlled physiology of reproduction in microbes, which is clearly linked to antibiotic resistance, has been discounted by evolutionary theorists who have touted pseudoscientific nonsense about mutations and natural selection in the context of evolution and biodiversity.

We now see an accurate representation by Carl Zimmer (above) of how ecological variation in the supply of nutrients enables biophysically constrained ecological adaptations in species from microbes to man via conserved molecular mechanisms.

James Shapiro seems to already have implied that DNA uptake enables ecological adaptations in the context of natural genetic engineering. However, like other theorists who have failed to provide experimental evidence of mutation-driven evolution, Shapiro did not detail the mechanisms that enable either evolution or ecological adaptations. Will Carl Zimmer detail the mechanisms that enable mutations to cause evolution after his refutation of mutation-driven evolution in the context of antibiotic resistance?

Of course not! A day later, he’s touting mutation-driven evolution again. 

The Case for Junk DNA

Excerpt: “…it is imperative that those who claim that the vast majority of intergenic transcription is functional test their hypotheses. In the absence of this evidence, the declaration that we are in the midst of a paradigm shift with regards to eukaryotic genomes and gene expression [120] seems premature.”

Reported as

The Case for Junk DNA

by Carl Zimmer  5/9/14

Excerpt 1): “If a mutation alters junk DNA, it doesn’t do any harm because the junk isn’t doing us any good to begin with.”

Excerpt 2): “Even if ninety percent of the genome does prove to be junk, that doesn’t mean the junk is unimportant to our evolution. As I wrote last week in the New York Times, it’s from these non-coding regions that many new protein-coding genes evolve.”

My comment: Zimmer’s  story line becomes progressively more difficult to understand. One day, he inadvertently supports natural genetic engineering in the context of antibiotic resistance. The next day, he tells us that mutation-altered junk DNA may be important to our evolution, and cites his article about new protein-coding genes that somehow evolved.

Did genes for antibiotic resistance evolve in bacteria? NO!

Does any experimental evidence of biologically-based cause and effect suggest that new protein-coding genes evolve from junk DNA? NO!

Does natural genetic engineering explain antibiotic resistance in the context of ecological variation and nutrient-dependent pheromone-controlled ecological adaptations. YES!

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

How can it be “…imperative that those who claim that the vast majority of intergenic transcription is functional test their hypotheses,” when ideas about mutations, natural selection, and evolution have never been supported by experimental evidence and the claims of theorists continue to be based on the untested null hypothesis?

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Sex differences: demand explanations of the mechanisms

May 8, 2014 | James Kohl

What is the point of spotting sex differences if science cannot explain them?      

Excerpt: “Why don’t we demand explanations of the mechanisms that produce observed sex differences?”

My comment: As we indicated in our 1996 Hormones and Behavior review, sex differences are nutrient-dependent and pheromone-controlled at the advent of sexually differentiated cell types in yeasts.

Conserved molecular mechanisms and the mammalian model of hormone-organized and hormone-activated sex differences in behavior were subsequently extended to invertebrates and to life history transitions in the honeybee model organism.

Using the honeybee model organism as the link from microbes to humans, I reviewed what was known about the biological basis for differences in morphological and behavioral phenotypes in species from microbes to man in Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors

I then provided examples of how nutrient-dependent DNA methylation leads to amino acid substitutions that differentiate cell types in individuals of different species in my most recent published work: Nutrient–dependent / pheromone–controlled adaptive evolution: a model.

All the details of biologically based cause and effect in the context of nutrient-dependent pheromone-controlled cell type differentiation have become clear from the perspectives of physics, chemistry, and conserved molecular mechanisms. However, since evolutionary theorists cannot explain how mutations and natural selection led to the evolution of sex differences, they are motivated to keep serious scientists from explaining the fact that sex differences in cell types and in organisms from species of yeasts to mammals result from ecological variation and nutrient-dependent pheromone-controlled ecological adaptations. There’s a model for that!

Why haven’t you learned more about the model? One reason is that reviewers refused to review the submission of the manuscript I subsequently posted to figshare.com

This was an invited review: Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems

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Adaptive radiations vs pseudoscientific nonsense

May 7, 2014 | James Kohl

Rates of Dinosaur Body Mass Evolution Indicate 170 Million Years of Sustained Ecological Innovation on the Avian Stem Lineage

Excerpt: ‘One possible explanation of how this diversity evolved is the “niche filling” model of adaptive radiation—under which evolutionary rates are highest early in the evolution of a group, as lineages diversify to fill disparate ecological niches.”

Reported as 

Shrinking helped dinosaurs and birds to keep evolving

Excerpt: “The evolutionary line leading to birds kept experimenting with different, often radically smaller, body sizes — enabling new body ‘designs’ and adaptations to arise more rapidly than among larger dinosaurs. Other dinosaur groups failed to do this, got locked in to narrow ecological niches, and ultimately went extinct.”

My comment: In the context of ecological variation and adaptations, the authors accurately claim that: “Much of extant biodiversity may have arisen from a small number of adaptive radiations…” Compare that statement to this misrepresentation: “…genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world.” — Masatoshi Nei (2013).

To confirm the accuracy of the claim for adaptive radiations and extant biodiversity one need only look at the ecological adaptations associated with frugivory in mammals (e.g., in bats and in humans). Compare the ecological adaptations manifested in morphology and behavior, which are associated with the epigenetic effects of vitamin C on genome and phenome stability, to their basis in the ecological variation that led to ecological adaptations in birds.

The dinosaur-to-bird comparison introduces a component of missing heritability into what is currently known about biophysically constrained ecological adaptations. Simply put, the metabolism of food to species-specific pheromones controls the physiology of reproduction in all species and nutrient-dependent pheromone-controlled reproduction leads to species diversity. Therefore, to determine what happened to the dinosaurs, one need only look at nutrient-dependent variations in the morphological and behavioral phenotypes of white-throated sparrows, which are primarily associated with a difference in parental feeding behaviors. Bi-parental feeding is associated with morphological and behavioral phenotypes.

Clearly it is ecological, social, neurogenic, and socio-cognitive niche construction that underlies the ability to adapt to ecological variation in vertebrates like these sparrows, and in every species of invertebrate that ever existed. Those that did not ecologically adapt became extinct.

From experimental evidence in the white-throated sparrow morphs, we know that dinosaurs did not mutate into different species of birds. From experimental evidence in other species, we know that they did not mutate into existence. Thus, pseudoscientific claims that “constraint-breaking mutation” is responsible for biodiversity, may be supported by methods used in population genetics, but those claims are not supported with experimental evidence of biological facts in species from dinosaurs to birds, or in any extinct or ecologically adapted extant species. Ecological variation leads to nutrient-dependent pheromone-controlled ecological adaptations, not to mutation-initiated natural selection and evolution.

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