They suggest that deep evolution somehow conserved energy-dependent phosphorylation sites. The sites somehow link changes in the microRNA/messenger RNA balance from RNA-mediated cell type differentiation to morphological and behavioral diversity via amino acid substitutions in supercoiled DNA. But they do not mention chirality, autophagy, or supercoiled DNA in the context of molecular mechanisms that optimize microRNA activity in diverse species.
Reported on January 25, 2017 as: Partnering MicroRNAs & Targets in a Molecular Dance
The authors of the article and the science journalist fail to link an energy source to the molecular dance and they fail to link virus-driven energy theft to the end of the biophysically constrained dance.
My summary: Their failure to link changes in the speed of light on contact with water from chirality to energy-dependent RNA-mediated autophagy and biophysically constrained cell type differentiation exemplifies the failure of Precision Medicine to link nutrient energy-dependent endogenous RNA interference (RNAi) to healthy longevity and all biodiversity via metabolic networks and genetic networks to the physiology of reproduction.
Instead, the fact that RNAi targets exogenous genes in models of viral infection has been touted in the context of a “A Billion Dollar Baby in Therapy.” See: Get Well in the RNAi Way-RNAi, A Billion Dollar Baby in Therapy
See for comparison: Fire A (1999) RNA-triggered gene silencing.
Facts about ATP and the energy-dependent creation of RNA, which is required for gene silencing, seems to be missing from every aspect of energy-dependent gene activation and biophysically constrained RNA-mediated protein folding chemistry. See: DEPENDENCE OF RNA SYNTHESIS IN ISOLATED THYMUS NUCLEI ON GLYCOLYSIS, OXIDATIVE CARBOHYDRATE CATABOLISM AND A TYPE OF “OXIDATIVE PHOSPHORYLATION” (1964)
Fifty-two years later we have this representation of what is known
That representation can be compared to what is known about endogenous RNA interference and cell type differentiation in the context of virus-driven energy theft and all pathology.
Our stochastic modeling reveals that small changes in protein abundances can have large effects on MAPK activation. Additionally, data on protein turnover suggests that protein degradation plays an important role in regulating the pheromone pathway. Pheromone-stimulated degradation has been documented previously for the receptor (Ste2) (8), a regulator of G-protein signaling (Sst2) (9), components of the effector kinase cascade (Ste11, Ste7) 9., 10. and 11., and the transcription factor (Ste12) (12).
Bistability, Stochasticity, and Oscillations have been linked from femtosecond blasts of virucidal UV light to RNA-mediated DNA repair and cell type differentiation that links feedback loops from odors and pheromones to the physiology of reproduction in all living genera. That’s why all serious scientists are Combating Evolution to Fight Disease. That fact makes it difficult for me to accept any more claims about deep evolution.
See also: microRNA “amino acid”
Given the ease of finding supporting evidence that links nutrient-energy-dependent endogenous RNA interference to all cell type differentiation via natural selection for energy-dependent codon optimality and the physiology of reproduction, I wonder why Mendell’s group still touts “deep evolution” in the context of energy-dependent phosphorylation.