Excerpt: “…selected insects can be used as models for human diseases with an epigenetic component because the underlying molecular mechanisms (DNA methylation, histone acetylation and the expression of microRNAs) are evolutionarily conserved.”
My comment: Insect behavior is nutrient-dependent and pheromone-controlled. In my 2012 review, I concluded: Olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans (Keller et al., 2007; Kohl, 2007; Villarreal, 2009; Vosshall, Wong, & Axel, 2000). See: Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors
In my 2013 review, I noted that “…the epigenetic ‘tweaking’ of the immense gene networks that occurs via exposure to nutrient chemicals and pheromones can now be modeled in the context of the microRNA/messenger RNA balance, receptor-mediated intracellular signaling, and the stochastic gene expression required for nutrient-dependent pheromone-controlled adaptive evolution.”
I concluded that “Minimally, this model can be compared to any other factual representations of epigenesis and epistasis for determination of the best scientific ‘fit’.” See: Nutrient-dependent/pheromone-controlled adaptive evolution: a model.
The honeybee model organism was included: “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).”
Elekonich and Robinson (2000) linked our 1996 Hormones and Behavior review of RNA-mediated cell type differentiation to hormone-organized and hormone-activated behavior in insects. Elekonich and Roberts (2005) linked hormone-organized and hormone-activated behavior in insects to cell type differentiation during the life history transitions of the honeybee model organism.
We included a section on molecular epigenetics that linked yeasts to mammals via the physiology of their nutrient-dependent pheromone-controlled reproduction in From Fertilization to Adult Sexual Behavior.
What we now see, more than 18 years later, is another review article that links what is currently known about cell type differentiation to the microRNA/messenger RNA balance.
The question arises: Will any evolutionary theorist or “big bang’ cosmologist admit that they have missed what is arguably the most important contribution to Combating Evolution to Fight Disease? If so, will they also admit that their theories about biologically-based cause and effect are still nothing more than pseudoscientific nonsense that has contributed to the suffering and death of millions? Could most of that have been prevented if theorists had looked for experimental evidence that linked the microRNA/messenger RNA balance or that supported their use of de Vries definition of mutation and assumptions about how mutations could be linked to the evolution of biodiversity?
See: Replace the Modern Synthesis (Neo-Darwinism): An Interview With Denis Noble “[W]hat Haldane, Fisher, Sewell Wright, Hardy, Weinberg et al. did was invent…. Evolution was defined as “changes in gene frequencies in natural populations.” The accumulation of genetic mutations was touted to be enough to change one species to another…. Assumptions, made but not verified, were taught as fact.”
These assumptions continue to plague serious scientists. See for example: Evolutionary history of honeybees revealed by genomics
Excerpt: The researchers also identified specific mutations in genes important in adaptation to factors such as climate and pathogens, including those involved in morphology, behaviour and innate immunity.
My comment: The honeybee model organism cannot serve as a model for mutations and for adaptations via amino acid substitutions linked to the stability of protein folding in the organized genomes of species from microbes to man because mutations perturb protein folding.
The assumptions of researchers about mutations, which were made based on the de Vries century old definition of “mutation,” should have ended ~ 50 years ago, when Dobzhansky first noted that “Ingram and others found that hemoglobin S differs from A in the substitution of just a single amino acid, valine in place of glutamic acid in the beta chain of the hemoglobin molecule.” Biology, molecular and organismic
The hemoglobin S variant exemplifies a nutrient-dependent ecological adaptation to the presence of malarial parasites. Dobzhansky (1973) told us about another variant: “…the so-called alpha chains of hemoglobin have identical sequences of amino acids in man and the chimpanzee, but they differ in a single amino acid (out of 141) in the gorilla.” Nothing in Biology Makes Any Sense Except in the Light of Evolution
Nothing makes sense about cell type differentiation if it is placed into the context of beneficial mutations instead of nutrient-dependent RNA-directed DNA methylation and RNA-mediated amino acid substitutions that differentiate cell types. Researchers continue to tout the pseudoscientific nonsense of evolutionary theory at the same time the biologically-based cause of cell type differentiation has been thoroughly detailed.
See any of my published works and also see the most recent refutations of the pseudoscientific nonsense touted by evolutionary theorists:
All the above include predictions made in this Substantial excerpt from a review published in NATURE, March 2, 2000.
Video: ISHE Summer Institute 2013
Despite two decades of details, some researchers continue to report their findings in the context of mutations and adaptations, which are manifested as RNA-mediated changes in innate immunity, morphology, and behavior in species from microbes to man. They are biologically uniformed. See for example:
Excerpt: “What emerged was dark matter and its emergence involved the emergence of all the others. Hens and eggs emerged simultaneously.”
Excerpt: “This interpretation of thermodynamical criticality would mean that living system by definition live at the borderline of life and death!”
My comment: Living at the borderline of life and death is what all organisms do. If they can’t find food, they die.
See for comparison:
Abstract: 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. Species diversity is a biologically-based nutrient-dependent morphological fact and species-specific pheromones control the physiology of reproduction. The reciprocal relationships of species-typical nutrient-dependent morphological and behavioral diversity are enabled by pheromone-controlled reproduction. Ecological variations and biophysically constrained natural selection of nutrients cause the behaviors that enable ecological adaptations. Species diversity is ecologically validated proof-of-concept. Ideas from population genetics, which exclude ecological factors, are integrated with an experimental evidence-based approach that establishes what is currently known. This is known: Olfactory/pheromonal input links food odors and social odors from the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man during their development.