Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems
Abstract excerpt:
… 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… manifested in increasing organismal complexity…
My comment: The increasing organismal complexity attributed to microRNAs is manifested in the learning abilities and in the memory of different species.
See: microRNAs That Promote or Inhibit Memory Formation in Drosophila melanogaster, which was reported as:
Small RNAs found to play important roles in memory formation
Excerpt:
A number of studies have shown that miRNAs are critical for normal development and cellular growth and may contribute to the complexity of neurodegenerative diseases.
See also:
Understanding why animals are healthy offers path to precision medicine
Excerpt:
“In the end, it looks like you can shield mutations with a single change elsewhere in the same gene, creating a single champion.” Katsanis added.
My comment: In the end, evolutionary theorists seem destined to view nutrient-dependent RNA-directed DNA methylation and RNA-mediated amino acid substitutions that stabilize the organized genomes of all genera as if one mutation that perturbed RNA-mediated protein folding was paired with another mutation that was beneficial. The fact that these theorists cannot understand the difference between a mutation and an RNA-mediated amino acid substitution makes it impossible for them to understand anything about healthy cell type differentiation in any species. They would rather continue to portray pathology and health in the context of mutations and/or natural selection and the evolution of biodiversity.
See also:
Nutrient-dependent/pheromone-controlled adaptive evolution: a model
Excerpt:
The honeybee already serves as a model organism for studying human immunity, disease resistance, allergic reaction, circadian rhythms, antibiotic resistance, the development of the brain and behavior, mental health, longevity, diseases of the X chromosome, learning and memory, as well as conditioned responses to sensory stimuli (Kohl, 2012).
My comment: Animal models link RNA-mediated cell type differentiation to nutrient-dependent DNA repair via nutrient-dependent microRNAs. Animal models link viruses to entropic elasticity via viral microRNAs.
The anti-entropic epigenetic effects of nutrient-dependent microRNAs on DNA repair and healthy biodiversity appear to be ignored by theorists who cannot understand how nutrient-dependent metabolic networks are linked to genetic networks and the health or pathology of different species.
See, for comparison, what serious scientists have learned about the obvious epigenetic links from nutritional epigenetics to pharmacogenomics.
Clinically Actionable Genotypes Among 10,000 Patients With Preemptive Pharmacogenomic Testing
See also:
Why Trust a Theory? Reconsidering Scientific Methodology in Light of Modern Physics
Excerpt:
Can a high degree of trust in an empirically unconfirmed or inconclusively confirmed theory be scientifically justified? Does the extent to which empirically unconfirmed theories are trusted today constitute a substantial change of the character of scientific reasoning?
My comment: The list of speakers includes: George Ellis (University of Cape Town) and Joseph Silk (Johns Hopkins University and Universite Pierre et Marie Curie) who co-authored Scientific method: Defend the integrity of physics. We are rapidly approaching the time when the evolution industry and the “big bang” cosmology industry will be forced by other serious scientists to prove their theories or abandon them along with all the pseudoscientific nonsense that has been used to support ridiculous claims.