Random mutations and resulting evolution?

In the context of  Random Mutations in E. Coli and the Resulting Evolution On 7/15/2013 7:07 PM, clarence_sonny_williams wrote:

Mr. Kohl, it appears to me that your paper, “Nutrient-dependent . . .” [i.e., Nutrient-dependent / Pheromone-controlled thermodynamics and thermoregulation] has mischaracterized the research paper it cites.  Here is a link for Blount, Barrick Davidson & Lenski, 2012 , and I can find no discussion that bears reasonable resemblance to your comments in regard to that paper.  In short, it appears you concocted something and cited Blount et al in support of it, which appears to be in error.  I am not accusing you of fraud, but I urge you to be specific and explain how what you wrote in your paper is derived from Barrick et al, 2012.  I know that your paper was self-published and not subject to standard peer-review processes, but some standards should still apply when you cite a paper.

I am willing to devote the time necessary to verify that your published paper has properly cited other material, so your cooperation is appreciated.

What I wrote was not derived from Blount, et al (2012). Thus, the important issue is that Williams may not know “…a primary epigenetic signature is reinforced by secondary and tertiary repressive organization: intrachromosomal compaction and interchromosomal aggregation of OR genes in OSNs. The importance of this elaborate arrangement is shown by the disruption of these aggregates, which results in violation of monogenic OR transcription and coexpression of a large number of ORs.” Not knowing anything about this, which explains how the epigenetic landscape becomes the physical landscape of DNA via alternative splicings and epistasis, may be what makes Williams think I mischaracterized the research results from Genomic analysis of a key innovation in an experimental Escherichia coli population. There is no explanation for why he thinks that random mutations in E. coli would result in evolution.

The problem is typical. People who know relatively nothing about the basic principles of biology and levels of biological organization required to link cause and effect across species, are prone to assumptions about the use of citations that support the model in the context it is presented. The context includes hundreds of works not cited that have helped establish what is currently neuroscientifically known (e.g., about de novo creation of genes, which is how the epigenetic landscape is manifested in organization of the genome in different species). Thus, while it may seem reasonable for Williams to offer to verify proper citations in my unpublished work, it is unreasonable for him to first take a citation out of its context, infer that I concocted something, and also infer that I indiscriminately supported it.  This is typically done by the uninformed who are not qualified to verify that anyone else has properly cited anything.

Clearly, Williams knows nothing about “…the multi-step origin of nutrient use (citrate) in E. coli where gene duplications produce new functions by promoter capture events that change gene regulatory networks in what was described as a 1-2-3 process…“. This 3-step process was exemplified in Blount et, al., 2012 via the use by E. coli of citrate, which is why I cited that work. If Williams and people like him knew anything about such things, they would realize that mutation-driven evolution is a comparatively impotent (i.e., unimportant) approach to any 1-2-3 process that results in use of a novel nutrient source in accordance with Darwin’s ‘conditions of life.’ Three simultaneous mutations would be required. For contrast, by default, Darwin addressed the fact that organisms need to naturally select food so that they can reproduce. Thus, I reject the offer by Williams to review anything I have written for proper citation use. Instead, I encourage him to read my most recent peer-reviewed journal article (or anything that does not tout or attempt to support mutations theory) and compare my model of adaptive evolution to theories of mutation-driven evolution. For example, Williams brought to the attention of the human ethology group: Wielgoss et al 2013  with a quote “Mutations are the ultimate source of heritable variation for evolution.” He added,  “I am not aware of any respected biologist who disagrees with this statement, although I am familiar with some religiously-based groups who refuse to believe such things even in the face of innumerable scientific observations.” I know. By now you are asking yourself: “What kind of fool says things like that in an open forum for public discussion?”

Clearly, Williams exemplifies the type of fool whose beliefs about religiously-based groups cloud his perspective on what he thinks are innumerable scientific observations, which evidently are not going to be cited by him. That’s why I welcome the involvement of others in attempts to determine what Williams is not citing and whether it has any scientific merit whatsoever. I’m certain it is long past time to abandon mutations theory and accept the biological facts, which begin with the three steps required for nutrient uptake in species from microbes to man (not with a mutation). From the perspective of Blount et al (2012) “This three-step process—in which potentiation makes a trait possible, actualization makes the trait manifest, and refinement makes it effective—is probably typical of many new functions.” See also: Parallel Evolutionary Dynamics of Adaptive Diversification in Escherichia coli. Hold comments on their use of the term mutation until you understand the differences in context and concepts.

That concept from my model is  represented by Panksepp in the context of affective processing associated with nutrient acquisition and the gene, cell, tissue, organ, organ-system pathway. Clearly, this concept is the foundation for secondary-process learning and memory mechanisms, which interface with tertiary-process cognitive-thoughtful functions and behavior (Panksepp, 2011).  See for review: Cross-Species Affective Neuroscience Decoding of the Primal Affective Experiences of Humans and Related Animals   — but only if you believe that nutrient acquisition is a primary affective experience. Do not bother to even scan works like that if you think the concept of mutations is the foundation for anything neuroscientifically known.

Here’s what is known about how to link the sensory environment directly to adaptively evolved behaviors in mammals. There are 7 steps: (1) food odors and pheromones; (2) GnRH; (3) LH; (4) steroidogenesis and feedback; (5) white matter/gray matter development; (6) hippocampal neurogenesis; (7) learning and memory; and these steps lead to differences in behavior.

The biological basis for affective processing is demonstrable in the aforementioned bottom-up sequence, which incorporates what is currently known about the conserved molecular mechanisms in species from microbes to man that link nutrient metabolism to species-specific pheromones that control reproduction. Hopefully, people like Williams will see why claims of mutation-driven evolution are silly, which is largely because they do not address any physiological links across species like the aforementioned links I incorporated into my model of adaptive evolution (in my 2012 publication: Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors).

What amazes me is that someone like Williams, an aging 60-ish newly-returned-to-college type, thinks he has learned enough in a few semesters to challenge what I have learned during a 39-year career in the lab as a medical laboratory scientist. What kind of fool…? That was a rhetorical question.

Author: James Kohl

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