Re-interpreting long-term evolution experiments — Is delayed adaptation an example of historical contingency or a consequence of intermittent selection?
Excerpt: “… the series of events used to explain adaptation in the short-transfer LTEE (and in speciation) might need to be revised. The amplification model supported by this article has already be proposed as a means of evolving new genes (1) and has been experimentally shown capable of generating a novel genetic function within as few as 3000 cell generations (11). Both of these processes are arguably more difficult to achieve than the ability to activate a single silent gene.”
My comment: In species from microbes to humans, physics and chemistry are linked to gene activation, the de novo creation of new genes, adaptation, and speciation by energy-dependent hydrogen-atom transfer in DNA base pairs in solution.
Nutrient-dependent microRNA flanking sequences help to ensure that adaptations and speciation occur only in the context of the physiology of reproduction, which links the nutrient-dependent pheromone-controlled biophysically constrained chemistry of RNA-mediated protein folding to cell type differentiation in all living genera via protection against virus-driven genomic entropy.
Species-specific cell type differentiation is linked from supercoiled DNA to biodiversity via chromosomal rearrrangements — not by mutations and evolution.
The primary message of the paper by Van Hofwegen et al.is that Lenski’s experiments clearly show that ecological variation leads to biophysically constrained ecological adaptation in the context of Darwin’s “conditions of life.” Any other interpretation of the results must involve the mathematical models, inferences, definitions, and assumptions of pseudoscientists who invented neo-Darwinism.
Reported as: Similar Data, Different Conclusions
By tweaking certain conditions of a long-running experiment on E. coli, scientists found that some bacteria could be prompted to express a mutant phenotype sooner, without the “generation of new genetic information.” The resulting debate—whether the data support evolutionary theory—is more about semantics than science.
Excerpt 1) “The resulting debate—whether the data support evolutionary theory—is more about semantics than science.”
My comment: Science has put an end to the semantics, and all serious scientists know that. No data from any experiment that links atoms to ecosystems has ever supported neo-Darwinian theory.
Here, they try to equate the pseudoscientific nonsense touted by Lenski’s idiot minions with what is known to serious scientists about energy-dependent biophysically constrained RNA-mediated protein folding chemistry. For example, thermodynamic cycles of protein biosynthesis and degradation link hydrogen-atom transfer in DNA base pairs in solution from ecological variation to ecological adaptation in all living genera via the physiology of reproduction.
Excerpt 2) “When natural selection—that is, differential survival and reproduction—favors bacteria whose genomes have mutations that enable them to grow on citrate, those mutations most certainly provide new and useful information to the bacteria,” Lenski and Blount countered in their blog post. “To say there’s no new genetic information when a new function has evolved (or even when an existing function has improved) is a red herring that is promulgated by the opponents of evolutionary science.”
My comment: Differential survival and reproduction is nutrient-dependent and pheromone-controlled in species from microbes to humans. Serious scientists do not put that fact into the context of evolutionary science. Nutrient-dependent de novo gene creation is required for experience-dependent RNA-mediated receptor-mediated morphology and behavior to link supercoiled DNA to protection from virus-driven entropy of organized genomes in all genera. Without the protection of supercoiled DNA, there is no sequence of events that links neo-Darwinian theory from ecological variation to ecological adaptations manifested in the stability of organized genomes. The sequence of events MUST link atoms to ecosystems via differential survival and reproduction, not via mutations linked to pathology and entropy.
See also: Evolutionary Rewiring
My comment: Next, the term “mutation” can be placed into the context of semantics vs science. That will makes it clear that RNA-mediated DNA repair via nutrient-dependent amino acid substitutions underlies all links from atoms to ecosystems in the context of what is known to serious scientists about the physiology of reproduction.
This atoms to ecosystems model of ecological adaptations links nutrient-dependent epigenetic effects on base pairs and amino acid substitutions to pheromone-controlled changes in the microRNA / messenger RNA balance and chromosomal rearrangements. The nutrient-dependent pheromone-controlled changes are required for the thermodynamic regulation of intracellular signaling, which enables biophysically constrained nutrient-dependent protein folding; experience-dependent receptor-mediated behaviors, and organism-level thermoregulation in ever-changing ecological niches and social niches. Nutrient-dependent pheromone-controlled ecological, social, neurogenic and socio-cognitive niche construction are manifested in increasing organismal complexity in species from microbes to man.
…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).”
Combating Evolution to Fight Disease
My comment: (1 of 4)
“An alternative theory proposes environmentally induced change in an organism’s behavior as the starting point (1), and “phenotypic plasticity” that is inherited across generations through an unspecified process of “genetic assimilation” (2).”
This is now more than merely an alternative theory of genetic assimilation. It links transgenerational epigenetic effects from nutrient uptake and RNA-mediated events to amino acid substitutions that differentiate the cell types of all cells in all individuals of all organisms. See, for example: Starvation-Induced Transgenerational Inheritance of Small RNAs in C. elegans
The nutrient stress-induced RNA-mediated events, which link the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man, also link morphological and behavioral diversity via conserved molecular mechanisms exemplified in the context of biologically plausible ecological speciation in nematodes.
See: System-wide Rewiring Underlies Behavioral Differences in Predatory and Bacterial-Feeding Nematodes
A difference in their feeding behavior and in the anatomy of their mouth parts is linked from nutrient-dependent pheromone-controlled feedback loops to ecological, social, and neurogenic niche construction. The change in focus from mutations, natural selection, and the evolution of biodiversity via unknown evolutionary events to nutrient-dependent pheromone-controlled RNA-mediated events that differentiate cell types may be required for others to realize the difference between evolutionary theories and biologically-based facts about RNA-mediated events.
RNA-mediated events are biophysically constrained, which means they are a biologically plausible way to link the physics and chemistry of protein folding to increasing organismal complexity via molecular biology. RNA-mediated events can also be compared to any unknown evolutionary events that might arise in the context of an alternative theory about constraint-breaking mutations, or other theories that include no mention of RNA-mediated events.