Stress-linked population-level history dependence

By: James V. Kohl | Published on: March 11, 2016

The Science of President Trump

My comment: Trump is not a president. He may be the Republican front-runner. In any case, attempts to portray him as a president in the context of “science” must be viewed in the context of pseudoscientific nonsense and media misrepresentations. Many political views on science are unrealistic because they are based on the pseudoscientific nonsense touted by neo-Darwinian theorists. If someone thinks that nutrient-dependent pheromone-controlled multicellularity automagically evolved, their thought processes have probably already been subjected to stress-linked pathology caused by the viruses that prevent healthy longevity. Stress-linked pathology links cell type differentiation from single-celled organisms to other primates and to humans via the conserved molecular mechanisms of biologically-based cause and effect. See for example:

Response of single bacterial cells to stress gives rise to complex history dependence at the population level


Investigating how the behavior of single cells scales up to history dependence at the population level is an important goal. Many microorganisms live in dynamic environments where the quality and quantity of nutrients and biological, physical, and chemical stressors change continuously. Therefore understanding how microorganisms operate in such dynamic environments is a fundamental question. In addition, such understanding also has potentially relevant applications, for example in the context of pathogens that are exposed to fluctuating concentrations of antibiotics during treatment or microorganisms in technical systems that are exposed to dynamic operating conditions. Single-cell measurements help to achieve a deeper understanding of history-dependent processes in microbial populations.

My comment: Investigating the behavior of single cells leads to wrong conclusions when the energy required for the behavior is not considered. Neo-Darwinists typically do not consider the energy-dependent hydrogen-atom transfer in DNA base pairs in solution that is required to place the continuously changing “…quality and quantity of nutrients and biological, physical, and chemical stressors…” into the perspective of supercoiled DNA, which links metabolic networks and genetic networks from atoms to ecosystems in all living genera. For example, supercoiled DNA protects our organized genomes from virus-driven energy theft that links stress from effects on learning and memory to neurodegenerative diseases, such as Alzheimer’s.

See also: Division of labour and the evolution of multicellularity

In conclusion, in this paper we present a model showing that multicellularity and cellular differentiation can develop when cells can form an aggregate that enables them to exchange chemical signals and metabolites. This aggregate essentially has a higher physiological dimension, so that when there are cellular processes that are incompatible in a single cell, segregation of these processes into separate cells is possible in the aggregate form. Regulatory mechanisms that can control such a division of labour within an aggregate can be expected in many ancestral unicellular forms and are based on signals coming either from the cell itself, or from partner cells in the aggregate environment. The resulting division of labour can generate fitness benefits that lead to selection on the propensity of cells to aggregate, and hence to form multicellular and differentiated organisms.

My comment: They fail to include any facts about how the innate immune system. Their conclusion links the energy-dependent exchange of chemical signals from nutrients and their metabolites to genetic networks that link regulatory mechanisms to the division of labor and multicellularity outside the context of biophysically constrained RNA-mediated protein folding chemistry and the nutrient-dependent stability of organized genomes.  In the first quarter of the last century, the stability of organized genomes was linked by Hugo de Vries definition of “mutation” to the jump-like changes in morphology that population geneticists and other biologically uninformed non-scientists could readily observe.  Assumptions about their observations led to the invention of neo-Darwinism, which made Darwin’s “conditions of life” secondary conditions. Natural selection was the primary consideration, which allowed claims to be made about mutations and evolution.
We now see what happens when anything is assumed without consideration for stress-perturbed “conditions of life.”  But, it’s too late.
The predictability of molecular evolution during functional innovation has repeatedly been placed into the context of biophysically constrained nutrient energy-dependent RNA-mediated DNA repair without acknowledging the role of  virus-driven pathology, which prevents ecological variation from linking Darwin’s “conditions of life” to ecological adaptation and all biomass and all biodiversity.
The energy-dependent predictability of hydrogen-atom transfer in DNA base pairs in solution, which links supercoiled DNA to protection against virus-driven entropy in all organisms with organized genomes, is missing in representations of molecular evolution that predictably must involve de novo gene creation and functional innovation.  When nutrient-dependent de novo gene creation and RNA-mediated DNA repair are not considered, what we have is an example of the magic of molecular evolution. If molecules automagically evolve, the molecules can be linked to the evolution of everything else. Proteins can evolve! Multicellularity can evolve! Sexually differentiated cell types can evolve! All cell type differences can evolve! People can evolve!
Evolution became predictable based on the ignorance of energy-dependent cell type differentiation that links hydrogen-atom transfer in DNA base pairs in solution to supercoiled DNA via nutrient-dependent RNA-mediated gene duplication and amino acid substitutions that repair virus-damaged DNA.  Cell type differentiation that is obviously controlled by the physiology of reproduction was removed from Darwin’s “conditions of life” and — before most people knew it — they were left with pseudoscientific nonsense based on a definition and the assumptions of the biologically uninformed.

Regaining the ability to grow in the absence of this gene requires the evolution of a new function that allows sufficient amounts of serine to be made to support cell growth. Although this experimental system does not necessarily recapitulate natural evolutionary scenarios, many aspects of this design are reflective of ecological and evolutionary features found in more natural circumstances.

See also: Serine
My comment: Serine is a protein-building amino acid.  Protein building requires controlled thermodynamic cycles protein biosynthesis and degradation. Although serine is not essential in the human diet because it is synthesized via typical intercellular interactions, the human ability to produce the amino acid serine and its effect on protein folding did not automagically arise in the absence of amino acid substitutions in other species that stabilized their genomes in the context of nutrient-dependent pheromone-controlled ecological adaptations.
If serious scientists had tried to link energy-dependent changes in base pairs to amino acid substitutions that prevent neurodegenerative diseases such as Alzheimer’s, most people would have focused on prevention and minimally expensive dietary supplements in attempts to prevent the stress-induced viral replication that has just been reported to cause Alzheimer’s.

See also:  Microbes and Alzheimer’s Disease

See also: On epigenetics: We are not just our DNA

My comment (awaiting moderation): Thanks for reporting on the symposium presentation.
In the early 1990’s Bruce McEwen told me to start with gene activation if I wanted anyone to validate my mammalian model. It developed into a model that now links energy-dependent hydrogen-atom transfer in DNA base pairs in solution from RNA-mediated DNA repair to supercoiled DNA that protects the organized genomes of all living genera from virus-driven entropy.
The symposium validated my model in the context of what has since been learned about transgenerational epigentic inheritance of the Zika virus, and the virus-driven pathology of Alzheimer’s disease.
Simply put, the nutrient-dependent innate immune system links RNA-mediated DNA repair to healthy longevity or virus-driven energy theft to all pathology via what is currently known about biophysically constrained protein folding chemistry and the physiology of nutrient-dependent reproduction.


Notify of
Inline Feedbacks
View all comments

Want more on the same topic?

Swipe/Drag Left and Right To Browse Related Posts: