See also: Epigenetics: microRNAs effect an integrative pathway for my additional comments on Master orchestrator of the genome is discovered, stem cell scientists report)
Retinoic acid is a metabolite of vitamin A (retinol) that mediates the functions of vitamin A required for growth and development.
The fibroblast growth factor receptor 1 “…gene provides instructions for making a protein called fibroblast growth factor receptor 1. This protein is one of four fibroblast growth factor receptors, which are related proteins that are involved in important processes such as cell division, regulation of cell growth and maturation, formation of blood vessels, wound healing, and embryonic development.”
The link from the epigenetic landscape to the physical landscape of DNA in the organized genomes of insects and mammals attests to the role that nutrient-dependent pheromone-controlled reproduction plays in ecological adaptations. Ecological variation links the availability of nutrients to biodiversity via ecological adaptations. Claims that species evolve are ridiculous in the context of what is known about the following 4 steps
1) the biophysically constrained chemistry of RNA-mediated protein folding that
2) links retinoic acid from vitamin A to
3) nutrient-dependent microRNAs and
4) the gene for fibroblast growth factor receptor 1 (FGFR1) to the honeybee model organism.
Those 4 steps link nutrient-dependent pheromone-controlled ecological adaptation from honeybees to humans.
Excerpt from Kohl (2013)
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).
In Kohl (2012), I cited
1) Differential gene expression between developing queens and workers in the honey bee, Apis mellifera, and I cited
2) Epigenetics: A New Bridge between Nutrition and Health in Kohl (2013).
Taken together the links from vitamin A to retinoic acid and the FGFR1 gene from nutrient-dependent microRNAs to cell type differentiation should be perfectly clear.
1) These proteins, all ≈130 amino acids in length, are universally present in vertebrates, where they appear to bind retinoic acid among other molecules.
2) Retinoic acid is involved in differentiation of embryonic stem cells as well as differentiation of various cancer cells in culture. Interestingly, a global decrease in H3K27 trimethylation was observed 3 d after differentiation of mouse embryonic stem cells induced by retinoic acid treatment.
2) MicroRNA can play important roles in controlling DNA methylation and histone modifications, creating a highly controlled feedback mechanism. Interestingly, epigenetic mechanisms such as promoter methylation or histone acetylation, can also modulate microRNA expression.
The two article I cited, link vitamin A and retinoic acid from nutrient-dependent microRNAs to RNA-directed DNA methylation and RNA-mediated amino acid substitutions that differentiate the cell type of insects and mammals. Stem cell differentiation is linked to behavior in mammals via the nutrient-dependent pheromone-controlled physiology of reproduction. RNA-mediated cell type differentiation via amino acid substitutions is also linked to the nutrient-dependent pheromone-controlled physiology of reproduction of microbes and insects.
See also: Gene-Nutrient Interactions and DNA Methylation
DNA methylation, both genome-wide and gene-specific, is of particular interest for the study of cancer, aging and other conditions related to cell-cycle regulation and tissue-specific differentiation, because it affects gene expression without permanent alterations in DNA sequence such as mutations or allele deletions. Understanding the patterns of DNA methylation through the interaction with nutrients is fundamental, not only to provide pathophysiological explanations for the development of certain diseases, but also to improve the knowledge of possible prevention strategies by modifying a nutritional status in at-risk populations.
Excerpt from the conclusion of 2) …it is very hard to delineate the precise effect of nutrients or bioactive food components on each epigenetic modulation and their associations with physiologic and pathologic processes in our body, because the nutrients also interact with genes, other nutrients, and other lifestyle factors. Furthermore, each epigenetic phenomenon also interacts with the others, adding to the complexity of the system.
My comment: The ability to link the precise epigenetic effect of vitamin A via retinoic acid and the FGFR1 gene links via nutrient-dependent microRNAs to RNA-mediated amino acid substitutions that differentiate the cell types of honeybees and humans during their life history transitions. For the link from the metabolism of nutrients from metabolic networks to genetic networks and human behavior during life history transitions see: Oppositional COMT Val158Met effects on resting state functional connectivity in adolescents and adults.
The Val158Met amino acid substitution links nutritional epigenetics to pharmacogenomics. That fact explains why publication of Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors , which was followed by publication of Nutrient-dependent/pheromone-controlled adaptive evolution: a model, led to this request from Justin M. O’Sullivan:
I am writing on behalf of myself, Prof. Lynnette Ferguson, as co-editors of a special issue of this journal on “Nutritional epigenetics”, scheduled to appear in 2014. We would like to invite you to write either a review for this issue of the journal, or consider publishing an original research article in the area.