Timothy Normand Miller (Digital circuit designer, software engineer, master debugger, computer engineering PhD, former college professor) @theosib2 wrote:
Adam Karaba (Assistant Professor, Department of Organic Technology, UCT Prague) @KarabaAdam wrote:
- I really dont like when anybody forces his faith into science, or issue his faith as a science. There is no place for such things in the science. It is not rational even ethic.
- Thank you for providing more point on my list – how to detect ‘bad’ ‘science’ for my lectures about science ethics.
- Just more and more trash without any meaning
My reply: I get that a lot. Perhaps you are also simply too stupid to put it into the context of this award-winning review of biophysically constrained RNA-mediated cell type differentiation across kingdoms.
See: Human pheromones: integrating neuroendocrinology and ethology 10/22/2001
…the biological basis for the development of physical attraction based on chemical signals is well detailed.
See also: A Paradigm for Peptide Hormone-GPCR Analyses 9/18/20
Our work utilized the yeast Saccharomyces cerevisiae as a model system for understanding peptide-GPCR interactions.
…deep insight can be gained into the structure and conformational dynamics of GPCR-peptide interactions in the absence of a crystal structure.
Biologically uninformed theorists placed that insight back into the context of neo-Darwinian pseudoscientific nonsense in Evolution of gonadotropin-releasing hormone (GnRH) structure and its receptor 3/15/12
It is very surprising and fascinating that the coordinated evolutionary selection of amino acids participating in binding GnRH has resulted in such perfection, that no substitution with a natural amino acid in any position improves binding potency.
For comparison, our insight linked everything known about energy-dependent RNA-mediated cell type differentiation to biophysically constrained viral latency and healthy longevity across kingdoms via the pheromone-regulated genetic processes of reproduction. See our Hormones and Behavior review: From Fertilization to Adult Sexual Behavior (1996) author’s copy.
For instance, a yeast pheromone, the alpha-mating factor, is very similar in structure to mammalian gonadotropic releasing hormone (GnRH). When injected into rats, this chemical binds to pituitary GnRH receptors and brings about the release of LH. Loumaye, Thorner, and Catt (1982) note: “GnRH and the yeast alpha-mating factor appear to represent a highly conserved effector system which includes the peptide ligand, the cell-surface receptor, and the physiological regulation of reproductive function” (p. 1325).
See also: Link opens .pdf …yeast α mating factor has 80% amino acid homology with mammalian GnRH…
An across-species continuum of top-down energy-dependent causation links achiral glycine in position 6 of the GnRH decapeptide hormone to biophysically constrained viral latency in all jawed vertebrates in the context of the conserved conformational dynamics of GPCR-peptide interactions in the yeast model organism.
Identification of the conformation-independent interhelical contact network has provided explanations for decreased expression of many cHH-associated mutant GnRH receptors, whereas the conserved conformation-specific interhelical contacts begin to explain how conserved residues mediate receptor activation. In spite of the diversity of ligand-binding surfaces, recent agonist-bound peptide-binding GPCRs suggest that ligand contacts in TM3 may trigger receptor activation and they may explain the high affinity of conformationally constrained GnRH peptides.
Update: Quorum sensing across bacterial and viral domains 1/7/21
…fungi, plant cells, and mammalian cells can synthesize AI mimics that modulate bacterial QS-controlled behaviors [39–42]. Eukaryotic host factors can likewise modulate QS via inactivation or sequestration of bacterial AIs [43–46]. The role of phages in phage–bacterial relationships and in three-way phage–bacterial–eukaryotic partnerships, both harmful and beneficial, represents an exciting research frontier. Given the prevalence of phages in bacterial communities combined with the prevalence of microbiome bacteria in and/or on eukaryotic hosts, defining the contributions of phages to QS could prove central to a comprehensive understanding of the functioning of QS in natural settings.
Both mutations introduce a mismatch within eight contiguous base-pairs, incurring large energetic penalties. For example, 6.4 kcal mol−1 would correspond to a change in the equilibrium binding constant by a factor of ~60,000 instead of ~2 as we observed. Therefore, Hfq must be buffering the effect of breaking internal base-pairs in short helices. How this is achieved is presently unknown.
The buffering is achieved via light-activated carbon fixation and energy-dependent changes in the microRNA/messenger RNA balance as predicted in:
…the epigenetic ‘tweaking’ of the immense gene networks that occurs via exposure to nutrient chemicals and pheromones can now be modeled in the context of the microRNA/messenger RNA balance, receptor-mediated intracellular signaling, and the stochastic gene expression required for nutrient-dependent pheromone-controlled adaptive evolution. The role of the microRNA/messenger RNA balance (Breen, Kemena, Vlasov, Notredame, & Kondrashov, 2012; Duvarci, Nader, & LeDoux, 2008; Griggs et al., 2013; Monahan & Lomvardas, 2012) in adaptive evolution will certainly be discussed in published works that will follow.
More than 117,600 indexed published works support that claim. See microRNA