Constrained evolution is ecological adaptation

By: James V. Kohl | Published on: January 13, 2015

See also: Unconstrained evolutionary innovability
Ideas that evolution is not constrained can be compared to experimental evidence of biophysically constrained ecological adaptations. The most recent relevant open access published work from the Jakobsson lab is: TRIM28 Represses Transcription of Endogenous Retroviruses in Neural Progenitor Cells. This is a link to a prior publication (also open access): microRNA-125 distinguishes developmentally generated and adult-born olfactory bulb interneurons
Taken together these two published works extend our 1996 model of RNA-mediated cell type differentiation to communication with human pheromones. See also: Chapter 16: Astrobiology: An Evolutionary Approach There is a link here to the book chapter “Language and Communication as Universal Requirements for Life.”
Excerpt: “Concepts such as genetic code, nucleic acid language, recognition sequences, translation process, amino acid language, immune responses, and cell–cell communication represent irreplaceable core concepts in molecular biology. These concepts were not introduced into biochemistry and molecular biology by linguists, communication experts, or language philosophers. Rather, they were independently coined by molecular biologists to explain observed phenomena and were clearly invoked due to the strong analogy to processes of human communication.”
Attempts to deny that these concepts extend across species seem foolish now that Andreas Wagner and Philip Ball have detailed how difficult it is for any of the integrated concepts to arise in the context of randomness. Indeed, even if it were only a matter of time and numbers of mutations, the evolution of anything seems impossible.
Unfortunately, the neo-Darwinists and the theistic evolutionists left themselves with no apparent “fall-back” position from which they could protect themselves. The fall-out from their ridiculous theories now rains down on them as if above-ground testing at the Nevada test site was still contributing to skin cancer in St. George, Utah. That pathology appears to occur in the context of an atoms to ecosystems model, but not the evolution of any species. Apparently, there has never been anything except ecological variation that leads to ecological adaptations that theorists thought arose via mutations and evolution.
John Hewitt addresses a problem with the definition of mutation in: Mitochondrial DNA mutations: The good, the bad, and the ugly
Excerpt: “The word ‘mutation’ is often associated with something negative, a disease causing variant or a pathogenic subsitution. The problem with these kinds of terms is that despite their different meanings, they can and will be used to describe the exact same change in any number of specific base pair alterations. This is no way to run scientific dialog, let alone research.”
My comment: Hewitt is unique among science journalists. He actually tries to understand what he’s reporting. Ask yourself why others haven’t noticed that no scientific dialogue occurs if the word ‘mutation’ means something negative, but also means something that is sometimes beneficial. How can the exact same change in any number of specific base pair alterations be described as a mutation that perturb protein folding and as a beneficial mutation? Hewitt reviews these two recently published works.
Mitochondrial DNA: Impacting Central and Peripheral Nervous Systems
Excerpt: “…mutations in mitochondrial DNA (mtDNA) cause energy production defects that frequently have severe neurological manifestations.”
Mitochondrial Genome Acquisition Restores Respiratory Function and Tumorigenic Potential of Cancer Cells without Mitochondrial DNA
Excerpt: “These results suggest pathophysiological processes for overcoming mtDNA damage and support the notion of high plasticity of malignant cells.”
My comment: Pretend you’re an evolutionary theorist. How do you differentiate between the mutations that cause energy production deficits and the mutations the help malignant cells overcome damage and continue contributing to pathophysiological processes associated with undifferentiated cell types?
Try this, link all mutations to perturbed protein folding and all amino acid substitutions to the stability of protein folding. That’s what serious scientists do. The fact that mutations are bad and amino acid substitutions are good helps serious scientists establish their scientific dialogues and run their experiments. Let a pseudoscientist into the lab, and next you will find them attempting to meaningfully interpret their meaningless results from mutagenesis experiments, as if some of the mutations were beneficial. See, for example: Lipid Encapsulation of Self Replicating Ribozymes. One of the most biologically uninformed science idiots I have ever encountered concludes:

Despite their challenges, ribozymes have made an interesting niche for themselves in the field of abiogenesis. The evolution of a successful RNA polymerase ribozyme is a lofty goal. While its discovery would not be the be-all and end-all of abiogenesis research, it would represent an important stepping stone between prebiotic chemistry and life. The encapsulation of such a ribozyme is also an important step, as it would enable a system of heredity and evolution through natural selection. Based on progress in current research, it is only a matter of time before that ribozyme is discovered.

How many times have you heard similar claims that researchers are just a few steps away from creating organisms that will evolve via mutations and natural selection?
Denis Noble provided a fitting antithesis to claims made by those who believe mutations and evolution explain what’s known about how ecological variation leads to ecological adaptations via the biophysically constrained chemistry of protein folding and RNA-mediated amino acid substitutions in species from microbes to man. He wrote: “Perhaps the elegant mathematics and the extraordinary reputation of the scientists involved blinded us to what now seems obvious: the organism should never have been relegated to the role of mere carrier of its genes.” Noble (2013)
See also: Evolution beyond neo-Darwinism: a new conceptual framework
Excerpt: In certain respects, my article reflects some of the points made over 30 years ago by Ho and Saunders (Ho and Saunders, 1979), who wrote: ‘The intrinsic dynamical structure of the epigenetic system itself, in its interaction with the environment, is the source of non-random variations which direct evolutionary change, and that a proper study of evolution consists in the working out of the dynamics of the epigenetic system and its response to environmental stimuli as well as the mechanisms whereby novel developmental responses are canalized.’
My comment: Noble cites “Beyond neo-Darwinism—an epigenetic approach to evolution.
Abstract except: “We argue that the basic neo-Darwinian framework—the natural selection of random mutations—is insufficient to account for evolution. The role of natural selection is itself limited: it cannot adequately explain the diversity of populations or of species; nor can it account for the origin of new species or for major evolutionary change. The evidence suggests on the one hand that most genetic changes are irrelevant to evolution; and on the other, that a relative lack of natural selection may be the prerequisite for major evolutionary advance.”
In 1979, we learned that natural selection of random mutations was not likely to account for evolution. In 2012, Andrew Jones claims: “The encapsulation of such a ribozyme is also an important step, as it would enable a system of heredity and evolution through natural selection.”
Obviously, something has gone horribly wrong. What could it be?
In his review of Wagner’s book, Philip Ball’s claims that “Natural selection supplies an incredibly powerful way of pruning variation into effective solutions to the challenges of the environment.
In his review of The Surprising Origins of Evolutionary Complexity Carl Zimmer claimed that “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.”
Statements like those can readily be placed into the context of what is currently known about epigenetic effects of nutrient uptake and the pheromone-controlled physiology of reproduction. For example, instead of starting with a definition of mutations and basing everything on assumptions about what they can do, we can start with this definition:
“Epigenetics: An essential mechanism for pruning down the wide range of possible behaviors permitted by genes, selecting those that fit an individual’s environment (Berreby, 2011).” cited in Kohl (2013)
By starting with a definition that integrates what is known about the biophysically constrained chemistry of protein folding and RNA-mediated events that link amino acid substitutions to cell type differentiation in species from microbes to man, we can arrive at accurate representations of biologically-based cause and effect that link ecological variation to ecological adaptations without the pseudoscientific nonsense of population genetics and neo-Darwinism.
See for additional information: Epigenetics in comparative physiology Most, if not all articles from this Special Issue of the Journal of Experimental Biology are open access.

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