The switch controls the growth of telomeres, the timekeepers of cells
September 19, 2014
Excerpt: Understanding how this “off” switch can be manipulated–thereby slowing down the telomere shortening process–could lead to treatments for diseases of aging (for example, regenerating vital organs later in life).”
My comment: Seemingly futile thermodynamic cycles of protein biosynthesis and degradation appear to be confusing. I’m somewhat certain that the folks at Salk realize that cycles of biophysically-constrained nutrient-dependent RNA-mediated protein folding limit how the switches are epigenetically-effected by olfactory/pheromonal input. I’m unsure that what they know is being conveyed to others.
This news report says nothing about how the conserved molecular mechanisms of nutrient-dependent, RNA-mediated, pheromone-controlled cell type differentiation via amino acid substitutions differentiates cell types in species from microbes to man during their life-cycle transitions.See for example:
The journal article is behind a paywall. I have requested it from the corresponding author and may be able to link “Regulated assembly and disassembly of the yeast telomerase quaternary complex” to the thermodynamics of protein structure and function from what they say about “The balance between the assembly and disassembly pathways, which dictate the levels of the active holoenzyme in the cell…” and homeostasis. Obviously, homeostasis is manifested in organism-level thermoregulation.
Hopefully, I can match what is known about biophysical constraints on light-induced amino acid substitutions to nutrient-induced amino acid substitutions in plants and animals via Single-residue insertion switches the quaternary structure and exciton states of cryptophyte light-harvesting proteins. The rest of the story can then be compared to the ‘Just-So’ stories of evolutionary theorists who left physics and chemistry out of their ridiculous theories based on population genetics.