Chance mutations — not natural selection

By: James V. Kohl | Published on: May 7, 2015

A Surprise for Evolution in Giant Tree of Life

Excerpt (with my emphasis):

Each variant adapted to suit a different ecological niche. But Blair Hedges, a biologist at Temple University in Philadelphia, has proposed a provocative alternative: Adaptation had little to do with it. It was simply a matter of chance and time.

See also: The Surprising Origins of Evolutionary Complexity July 16, 2013
Excerpt:

Some argue that life has a built-in tendency to become more complex over time. Others maintain that as random mutations arise, complexity emerges as a side effect, even without natural selection to help it along. Complexity, they say, is not purely the result of millions of years of fine-tuning through natural selection—the process that Richard Dawkins famously dubbed “the blind watchmaker.” To some extent, it just happens.

My comment: Variants do not adapt, and the complexity of systems biology did not just happen to arise. The epigenetic landscape is linked to the physical landscape of DNA via RNA-directed DNA methylation and RNA-mediated amino acid substitutions that differentiate the cell types of all genera via the fixation of amino acid substitutions in organized genomes, which occurs in the context of their physiology of their reproduction. Complexity is biophysically constrained by the nutrient-dependent chemistry of RNA-mediated protein folding, unless you are a theorist. See for instance: June 14, 2013 Mutation-Driven Evolution 
Conclusion:

…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).

See for comparison: June 14, 2013 Nutrient-dependent/pheromone-controlled adaptive evolution: a model
Conclusion:

…the largest contributor to the development of our personal preferences may be the unconscious epigenetic effects of food odors and pheromones on hormones that organize and activate behavior. If so, the model represented here is consistent with what is known about the epigenetic effects of ecologically important nutrients and pheromones on the adaptively evolved behavior of species from microbes to man. Minimally, this model can be compared to any other factual representations of epigenesis and epistasis for determination of the best scientific ‘fit’.

My comment: Carl Zimmer and Emily Singer are among the science journalists who have reported on the pseudoscientific nonsense about evolution that “just happens.” Ridiculous claims like that one have been replaced with each report that contains experimental evidence, which links ecological variation to nutrient-dependent ecological adaptations in all genera.

For example, in species from microbes to man, organisms adapt to ecological variation via fixation of RNA-mediated amino acid substitutions in their organized genomes. Fixation rapidly occurs in the context of their nutrient-dependent reproduction and the metabolism of nutrients to species-specific pheromones. Indeed, re-evolution of the bacterial flagellum reportedly occurred in four days. See: Evolutionary Rewiring: Strong selective pressure can lead to rapid and reproducible evolution in bacteria.

The surprise for evolutionary theorists is that natural selection of food, not chance mutations, enables ecological adaptations. That means their definitions and assumptions about how evolution occurs are useless left-overs from their biologically uninformed past.
Why do we keep seeing attempts to revise ridiculous theories, at the same time that serious scientists have learned how to link physics, chemistry, and molecular epigenetics to cell type differentiation and biodiversity in all genera? Could it be that most science journalists have been reporting only half of the information that is required for their target audiences to make informed decisions about biologically-based cause and effect? Could it be that they think their target audiences should remain biologically uninformed?
See also: Under the Sea, a Missing Link in the Evolution of Complex Cells
Excerpts:

Scientists have long known that mitochondria evolved from bacteria.
“This is a genuine breakthrough,” said Eugene Koonin, an evolutionary biologist at the National Center for Biotechnology Information who was not involved in the research. “It’s almost too good to be true.”

My comment: In 2005, Koonin co-authored A universal trend of amino acid gain and loss in protein evolution.
Excerpt:

We cannot conceive of a global external factor that could cause, during this time, parallel evolution of amino acid compositions of proteins in 15 diverse taxa that represent all three domains of life and span a wide range of lifestyles and environments. Thus, currently, the most plausible hypothesis is that we are observing a universal, intrinsic trend that emerged before the last universal common ancestor of all extant organisms.

My comment: This attests to the fact that the reported “genuine breakthrough” is “too good to be true.” If any species evolved from another species via mutations, which perturb protein folding,  serious scientists could claim that evolution was evidence of a miraculous population-wide transformation. Indeed, that transformation appears to have occurred in the four days it took to re-evolve the bacterial flagellum — as if there were no “Limits to adaptation along environmental gradients.”
Conclusion:

…the predicted emergence of inherent limits to species’ ranges across steadily varying environments offers extensions to the theory of ecological speciation and, eventually, may help us to elucidate macroecological patterns of biodiversity.

See also: Tracking niche variation over millennial timescales in sympatric killer whale lineages
Excerpt:

Ecological variation is the raw material by which natural selection can drive evolutionary divergence [1–4].

My comment: The microecological and macroecological patterns of biodiversity are linked from nutrient-dependent pheromone-controlled feedback loops and chromatin loops to chromosomal rearrangements and biodiversity. Serious scientists typically seem to think that the limits to the patterns are established by the availability of nutrient energy.
In the context of an atoms to ecosystems model, nutrient energy supplies the anti-entropic force that links viruses from entropic elasticity to speciation via RNA-directed DNA methylation and the RNA-mediated amino acid substitutions that differentiate cell types. Why aren’t science journalists reporting on that fact?
Even if they do not think that all experimental evidence links ecological variation to natural selection and chromosomal rearrangements, the evidence could be compared to opinions that have historically been based on assumptions about the definition of mutations and how they might be linked to evolutionary divergence if ever they were fixed in the organized genomes of any species. For example, if fixation of a mutation that was beneficial to all humans because it protected our species from malaria, it could be compared to the amino acid substitution that differentiates the blood cells of these primates. Dobzhansky (1973) “… the so-called alpha chains of hemoglobin have identical sequences of amino acids in man and the chimpanzee, but they differ in a single amino acid (out of 141) in the gorilla” (p. 127).
See also: Scientists reverse bacterial resistance to antibiotics
Excerpt:

Resistance to antibiotics is a natural part of the evolution of bacteria, and unavoidable given the many types of bacteria and the susceptibility of the human host.

My comments to the MedicalXpress.com site begin by addressing their foolish assumption:
Excerpt:

We have assumed that substitutions arise according to the strong selection weak mutation model (SSWM) [16] in which single substitutions reach fixation before the next substitution occurs.

My comment: Anyone who continues to avoid the experimental evidence that links RNA-mediated amino acid substitutions to cell type differentiation in all cells of all individuals of all genera will continue to be targeted by serious scientists who are Combating Evolution to Fight Disease.
For more information on how to join the combatants, see what is known to the USFDA about cell type differentiation in this list of variants linked from nutritional epigenetics to pharmacogenomics by enzymes and amino acid substitutions that link metabolic networks to genetic networks in all mammals.
Table of Pharmacogenomic Biomarkers in Drug Labeling
See also the difference that a single amino acid substitution can make in the context of behavioral development across the life history transition from adolescence to adulthood in humans. Oppositional COMT Val158Met effects on resting state functional connectivity in adolescents and adults and Tracking the Brain’s Functional Coupling Dynamics over Development.
Blair Hedges claims that that these adaptations arose as if “It was simply a matter of chance and time.” Science journalists who report that pseudoscientific nonsense should be forced to report what is known by serious scientists about cell type differentiation.
For example, what is known to serious scientists is now being taught in Israeli middle-schools. Israeli Middle Schools School to Include Theory of Evolution.
Excerpt:

“…learning about evolution is not the primary function of the decision, but rather to use it as a building block for students to learn more about their ecology.”

My comment: Elsewhere, students may still be taught to believe in the pseudoscientific nonsense about mutations, natural selection, and evolution — or about chance mutations without natural selection that are linked to evolution that “just happens.”


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