Tet3 regulates synaptic transmission and homeostatic plasticity via DNA oxidation and repair was reported as: Neurons constantly rewrite their DNA
Excerpt: “The scientists say they have discovered another mechanism used by neurons to maintain relatively consistent levels of synaptic activity so that neurons can remain responsive to the signaling around them. If synaptic activity increases, Tet3 activity and base excision of tagged cytosines increases. This causes the levels of GluR1 at synapses to decrease, in turn, which decreases their overall strength, bringing the synapses back to their previous activity level. The opposite can also happen, resulting in increasing synaptic activity in response to an initial decrease. So Tet3 levels respond to synaptic activity levels, and synaptic activity levels respond to Tet3 levels.”
My comment: They link nutrient-dependent RNA-directed DNA methylation from the complexity of links between metabolic networks and genetic networks to experience-dependent rewiring of the brain. RNA-mediated amino acid substitutions differentiate all cell types of all individuals of all genera, but that fact is not reported here. It is reported in the context of links from viral microRNAS and entropic elasticity to the anti-entropic epigenetic effects of nutrient-dependent microRNAs, but crossing disciplines is required to link the microRNA/messenger RNA balance to DNA repair.
See also: New insight into how proteins find their DNA binding sites in the genome
Excerpt: “When we talk about protein binding to DNA, we assume DNA is accessible, but in the cell it is folded up and covered by other proteins,” he said. “So the next step is to integrate information about cooperative binding and the accessibility of binding sites, going from the in vitro to the more complex in vivo situation. This also includes epigenetic mechanisms such as DNA methylation, which is another interest of my team.”
My comment: This was a report on publication of Quantitative modeling of transcription factor binding specificities using DNA shape. Again, the link from RNA-directed DNA methylation and RNA-mediated amino acid substitutions that differentiate all cell types is missing. What’s missing is critical to any model that attempts to link protein folding to functional protein structures. Minimally, however, the serious scientists that are reporting their links from DNA methylation to the organization of genomes are not mentioning the role of mutations and natural selection. Only evolutionary theorists continue to make that mistake. It’s a mistake because their misrepresentations of biologically-based cause and effect are clear to all but the most ignorant serious scientists.
Intelligent serious scientists have sided with creationists, who understand the difference between mutations and amino acid substitutions in the context of Tet-mediated DNA repair and 3D protein folding. See, for example: Three-Dimensional DNA Code Defies Evolution; Inching toward the 3D genome;
and see: Methyldynamics behind virtually all pathologies?
Excerpt: Epigenetic modifications shape behavior, modulate stress responsivity, and alter immune function. This facet of epigenetics seeks to understand the interactive linkages that connect the psychological and social environment with the epigenetic processes that modulate gene expression and influence behavior.
My comment: Anyone who does not yet realize that mutations are linked to pathology and amino acid substitutions are linked to nutrient-dependent DNA repair and the stability of organized genomes may need to review the extant literature. Starting with Dobzhansky (1973) for example, we see that: “…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” (p. 127). The only perspective that has changed during the past 4 decades is the one that links mutations to natural selection and the evolution of biodiversity. What’s changed is that serious scientists ignore the past claims of evolutionary theorists because serious scientists know the difference between mutations and amino acid substitutions — even if they do not detail those differences in their models.
The fact that Vitamin C induces Tet-dependent DNA demethylation and a blastocyst-like state in ES cells was reported on July 1, 2013 as Vitamin C helps control gene activity in stem cells.
The UCSF researchers demonstrated that Tet enzymes require vitamin C for optimal activity as they act to remove the methyl groups from the DNA and to stimulate gene activity that more faithfully mimics in cultured stem cells what occurs at early stages of development in the mouse embryo.”Potential roles for vitamin C in the clinic—including in embryo culture media used during in vitro fertilization, which currently do not contain vitamin C, and in cancers driven by aberrant DNA methylation—deserve exploration,” Ramalho-Santos, said
My comment: See also: Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems
In my invited review of nutritional epigenetics, I cited the work on vitamin C when I wrote:
Nutrient stimulation appears to change the structural integrity and functional significance of epigenetically stabilized hydrogen bonds via amino acid substitutions. This extends the effects of vitamins from the epigenetic landscape to receptor-mediated intracellular interactions and protein folding. The molecular mechanisms that enable this nutrient-dependent epigenetic stimulation appear to be conserved across phyla as diverse as amoeba and mammals (Hashimoto et al., 2013). Experimental evidence from studies of studies of amino acid substitutions and cell type differentiation (J. V. Kohl, 2013) suggests that a cascade of changes in protein structure and function may begin with a single vitamin-dependent base pair change (Blaschke, et al., 2013).
Two weeks before Blaschke et al. (2013) was published this ridiculous idea appeared in the conclusion of the textbook: 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.” The textbook and my review article: Nutrient-dependent/pheromone-controlled adaptive evolution: a model.
There is still no experimental evidence of biologically-based cause and effect that links mutations to the evolution of increasing organismal complexity via organization of genomes. The only link from ecological variation to ecological adaptation is nutrient-dependent RNA-directed DNA methylation, whether or not DNA methylation is linked to the RNA-mediated amino acid substitutions that stabilize the DNA of all organized genomes.