Stem Cells Remember Substrates
The stiffness of a culture substrate affects the fates of stem cells.
By Kerry Grens | March 16, 2014
Excerpt:” Earlier work has shown that stem cells respond to their physical environments, and studies have implicated the transcriptional coactivators YAP and TAZ in transducing this mechanical information from the environment to the cell.”
My comment: This report on transduction of mechanical information from the environment links the epigenetic landscape to the physical landscape of DNA in the organized genomes of cell types in individuals of different species. Information transduction appears to be biophysically constrained at the level of quantum physics and stem cell memory via the following sequence of events.
1) Vitamin-induced base pair “flipping” results in…
2) amino acid substitutions that…
3) stabilize the intracellular thermodynamic interactions required for…
4) protein folding, which result in…
5) nutrient-dependent de novo creation of cell types and…
6) maintenance of their diversity via the…
7) pheromone-controlled physiology of reproduction, which is responsible for…
8) ecological adaptations manifested in…
9) morphological phenotypes and in…
10) behavioral phenotypes.
Thus, ecological variation and ecological adaptations are manifested in vitamin-dependent morphological and behavioral phenotypes, which are associated with micronutrient-and macronutrient-dependent species diversity.
The fact that YAP inhibits miRNA biogenesis by a transcriptionally independent mechanism and also appears to contribute to oncogenic progression (see for review: Hippo Signaling Regulates Microprocessor and Links Cell-Density-Dependent miRNA Biogenesis to Cancer) also appears to clearly link YAP from vitamin-dependent changes in embryonic stem cells to their nutrient-dependent cell type differentiation in adult organisms.
Some evolutionary theorists attribute cell type differentiation in individuals and in species to constraint-breaking mutations that somehow enable increasing organismal complexity, and also enable disease processes, which lead to mental disorders in human populations. Personally, I find it unbelievable that anyone who is informed about the biology of cause and effect would believe that increasing organismal complexity manifested in species diversity is mutation-driven. That suggests all differences in human populations and differences in the cell types of other species exemplify the result of accumulated mutations instead of nutrient-dependent amino acid substitutions.
However, the magnitude of cause and effect attributed to vitamin D was only recently revealed. Vitamin D-mediated production of serotonin may be critical for the production of serotonergic signals during neurodevelopment. This indirectly links vitamin D to the development of the brain and changes in the brain associated with skull architecture and brain development throughout adulthood because serotonin plays a critical role in regulating a variety of brain functions, which include social behavior. Vitamin-dependent social behavior is not likely to be considered in the context of population genetics, which may be why the claim “We Are All Mutants” was recently attributed to the author of Mutation-Driven Evolution.
It seems likely to me that all individuals of all species are more or less ecologically adapted and that nutrient-dependent pheromone-controlled ecological adaptations can be perturbed by nutrient stress and social stress. With increasing organismal complexity, stress probably contributes to physical diseases and mental disorders via epigenetically-effected information transmission associated with learning and memory at the cellular level of quantum physics. Perhaps the increasing organismal complexity of human populations led population geneticists to attribute our ecological adaptations to constraint-breaking mutations. But, unless experimental evidence supports such claims, they should stop doing that.
