A National Institutes of Health-funded consortium publishes 111 reference maps of DNA and histone marks.
February 18, 2015|
“All our cells have a copy of the same book, but they’re all reading different chapters, bookmarking different pages, and highlighting different paragraphs and words.” These chemical bookmarks, such as methylation and acetylation, help control which genes are transcribed into RNA and expressed in a given cell type, thus aiding the maintenance of a particular cell’s identity.
My comment: Study coauthor Manolis Kellis may be the first to metaphorically explain nutrient-dependent RNA-directed DNA methylation and cell type differentiation in terms that non-scientists can understand. See also: Life is physics and chemistry and communication and Top-down causation: an integrating theme within and across the sciences? If all your bookmarks are in the texts from a specific discipline or area of expertise, you’re less likely to understand the importance of learning how ‘chemical bookmarks’ linked to mutations may lead to the failure of particular cell types to maintain their RNA-mediated identity.
For example, others have engineered genetically modified E. coli with a synthesized amino acid substitution that probably ensures the stability of DNA in its organized genome. See: Biocontainment of genetically modified organisms by synthetic protein design. Many theorists are only familiar with works by those who claim to have “bottled evolution.” See, for example: The Man Who Bottled Evolution. Lenski’s experiments are examples of how ecological variation in the food supply lead to ecological adaptations via conserved molecular mechanisms in species from microbes to man.
Now that others have brought forward the topic of how gene transcription and RNA are linked to the maintenance of a particular cell’s identity, it may be easier for others to grasp the fact that cell type identity is nutrient-dependent and pheromone-controlled.
Can anyone else help to explain how RNA-directed DNA methylation and RNA-mediated amino acid substitutions link the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man?
That explanation would help to rid serious scientists of claims that mutations somehow lead from entropic elasticity to anti-entropic stability. The stability is obviously due to the fixation of the amino acid substitutions in the context of the physiology of nutrient-dependent species-specific reproduction. That explanation of anti-entropic stability might also help alleviate fears that genetically modified organisms could lead to the death of us all.
The alternative to explanations of anti-entropic stability is to change Gregor Mendel’s century-old “law of segregation” and/or add more laws to the second law of thermodynamics in attempts to explain transmission ratio distortion (TRD).
Distortion links nutrient-dependent fixation of favored alleles from plants to animals via the biophysically constrained chemistry of RNA-mediated protein folding and the physiology of reproduction.
Facts about nutrient-dependent TRD could be compared to theories about the role that constraint-breaking mutations play in the evolution of biodiversity. See for example: Mutation-Driven Evolution “…genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world.” (p. 199)
Obviously, mutations contribute to transmission rate distortion (TRD). The question arises, how could they contribute to entropic elasticity and anti-entropic stability. Mutations are linked from perturbed protein folding to physiopathology, not to the physiology of reproduction that is nutrient-dependent and pheromone-controlled.