Autophagy (epigenetically effected by nutrient-energy and controlled by the physiology of reproduction)
See for comparison: Virus-driven energy theft and epigenetically-effected autophagy
The number of citations to published works that link the use of Selleck Chem products to the discovery of all aspects of all RNA-mediated theory killers suggests it is time to move forward.
So does this article from one of my trade publications:
See also: Immune repertoire analysis is gaining interest as a clinical NGS application By John Brunstein
The technique stems from looking at the patient’s adaptive immune system. In a much simplified explanation, this is the system whereby developing B and T cells undergo reclombination at defined genetic regions known as V – (D) – J (Variable, Diversity, and Joining) regions to develop unique antibodies and T cell receptors (TCRs) respectively. Based on their unique peptide sequences, these can create specific binding affinity for “non-self” ligands such as those present on pathogens or on transplanted organs. While such reassortment is essentially random in nature and thus constantly samples a wide range of “sequence space” or potential binding surfaces, those individual B and T cells whose recombinant markers find a “non-self” match are positively selected for and undergo clonal expansion as the basis for cell-mediated immunity.
My comment: Brunstein places everything known about energy-dependent hydrogen-atom transfer in DNA base pairs in solution back into a story about natural selection for energy-dependent codon optimality without mentioning that fixation of RNA-mediated amino acid substitutions is linked to the stability of supercoiled DNA in all living genera via the physiology of reproduction. He also fails to link microRNA flanking sequences to transgenerational epigenetic inheritance of all morphological and behavioral phenotypes via autophagy — as if he had never heard of it.
Our investigation demonstrates the utility of miRNA sequences as classical phylogenetic markers, and shows this usage is robust to different algorithms of phylogenetic analysis and the analysis of fast-evolving lineages. Such a method provides novel characters for assessing phylogenetic relationships that will be of use in a range of contexts for resolving branches across the tree of life.
My comment: The overwheming utility of miRNA sequences arises in the context of how the structure and function of the branches across the tree of life are created. The structure and function is energy-dependent and RNA-mediated via fixation of amino acid substitutions in supercoiled DNA, which protects all organized genomes from virus-driven entropy.
See also: Stat Profile Prime CCS Blood Gas Analyzer from Nova Biomedical (ad copy from one of my trade publications)
My comment: Measuring pH links virus-driven genomic entropy to all pathology. It also links nutritional epigenetics from the innate immune system to healthy longevity via everything known about virus-driven energy theft, which links stress from the replication of viruses to all pathology via critical care testing of other blood gas analytes such as pCO2, pO2, Sodium, Potassium, Chloride, Calcium, Glucose, Lactic Acid, and Hematocrit.
For information on how virus-driven theft of the sun’s anti-entropic virucidal quantised energy is linked to all pathology see:
Poster: The anti-entropic force of virucidal ultraviolet light links guanine–cytosine (G⋅C) Watson–Crick base pairing from hydrogen-atom transfer in DNA base pairs in solution to supercoiled DNA, which protects the organized genomes of all living genera from virus-driven entropy. For example, protection of DNA from permanent UV damage occurs in the context of photosynthesis and nutrient-dependent RNA-directed DNA methylation, which links RNA-mediated amino acid substitutions to DNA repair. In the context of thermodynamic cycles of protein biosynthesis and degradation, DNA repair enables the de novo creation of G protein coupled receptors (GPCRs). Olfactory receptor genes are GPCRs. The de novo creation of olfactory receptor genes links chemotaxis and phototaxis from foraging behavior to social behavior in species from microbes to humans. Foraging behavior links ecological variation to ecological adaptation in the context of this atoms to ecosystems model of biophysically constrained energy-dependent RNA-mediated protein folding chemistry. Protein folding chemistry links nutrient-dependent microRNAs from microRNA flanking sequences to energy transfer and cell type differentiation in the context of adhesion proteins, and supercoiled DNA that protects all organized genomes from virus-driven entropy.
I hope that scientific progress is not delayed by another 20-80 years because Yoshinori Ohsumi’s works failed to address anything known about how virus-driven energy theft causes mutations, which are linked to all pathology. There are still some pseudoscientists who link constraint-breaking mutations from energy-dependent viral latency to all biodiversity.
See for example: Mutation-Driven Evolution (p. 199)
… genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world. In this view of evolution there is no need of considering teleological elements.
My comment: How can someone who advocates ignoring everything known to serious scientists about teleology in the context of autophagy publish a textbook on evolution? Who has funded this nonsense since the time neo-Darwinian theory was invented?
See for comparison: Nutrient-dependent/pheromone-controlled adaptive evolution: a model
…the model represented here is consistent with what is known about the epigenetic effects of ecologically important nutrients and pheromones on the adaptively evolved behavior of species from microbes to man. Minimally, this model can be compared to any other factual representations of epigenesis and epistasis for determination of the best scientific ‘fit’.
Reported as: Differing division rates of brain stem cells
…human cells take more time to arrange the chromosomes before they are distributed to the daughter cells. This may help to understand why human and chimpanzee brains develop differently.
…gene expression differences between the species also hinted that proliferation capacity differs between the species. “The subtle but intriguing differences we have found at the cellular and molecular level may play important roles in the evolution of the human brain” concludes Wieland Huttner, who supervised the study. The researches will now focus on investigating the mechanisms and implications of these differences.
ARHGAP11B arose on the human evolutionary lineage after the divergence from the chimpanzee lineage by partial duplication of ARHGAP11A (25, 26), which is found throughout the animal kingdom and encodes a Rho GTPase-activating-protein (RhoGAP) (27, 28). ARHGAP11B exists not only in present-day humans but also in Neandertals and Denisovans (26, 29–31) (Fig. 2). ARHGAP11B contains 267 amino-acids and is a truncated version of ARHGAP11A, comprising most of the GAP-domain (until lysine-220) followed by a novel C-terminal sequence but lacking the C-terminal 756 amino acids of ARHGAP11A (Fig. 2 and fig. S10).
My comment: Dobzansky (1973) Nothing in Biology Makes Any Sense Except in the Light of Evolution linked the similarities and differences in gene expression from gorillas to chimpanzees and modern humans by a single amino acid substitution.
… 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).
Thomas Hunt Morgan’s model for the study of evolution won him the 1933 Nobel Prize in Physiology or Medicine for demonstrating that chromosomes act as the carriers of inheritance.
See also: Thomas Hunt Morgan
Morgan laid the foundation of the science of genetics. He also laid the theoretical foundation for the mechanism of evolution: natural selection. Heredity was a central plank of Darwin’s theory of natural selection, but Darwin could not provide a working theory of heredity. Darwinism could not progress without a correct theory of genetics. By creating that foundation, Morgan contributed to the neo-Darwinian synthesis, despite his criticism of Darwin at the beginning of his career.
My comment: The neo-Darwinian synthesis failed to link Darwin’s ‘conditions of life’ to chromosomes as the carriers of what is known to serious scientists as transgenerational epigenetic inheritance of all morphological and behavioral phenotypes. Conditions of life are nutrient energy-dependent and controlled by the physiology of reproduction in all living genera. Autophagy is the link from natural selection for energy-dependent codon optimality to the RNA-mediated amino acid substitutions that Dobzhansky claimed differentiated other species and the cell types of chimpanzees and modern humans from the cell types of gorillas.
If Morgan actually contributed anything to the neo-Darwinian synthesis, 2004 Nobel Laureates Richard Axel and Linda Buck removed his contributions by linking the de novo creation of olfactory receptor genes to cell type differentiation in all living genera. This year’s Nobel Laureate in Physiology or Medicine delivered the final blow to the “Modern Synthesis” with his works on autophagy, which link energy-dependent thermodynamic cycles of protein biosynthesis and degradation to healthy longevity and virus-driven energy theft to all pathology via the conserved molecular mechanisms of RNA-mediated protein folding chemistry, which have since been linked to supercoiled DNA via receptor-mediated behaviors.
See also: Send Your Brain Back in Time
Until recently, the conventional wisdom within the fields of neuroscience and psychiatry has been that development is a one-way street, and once a person has passed through his formative years, experiences and abilities are very hard, if not impossible, to change.
My comment: That is a lie. The fields of neuroscience and psychiatry have simply ignored everything known to serious scientists about plasticity.
See for example: Nutrient-dependent/pheromone-controlled adaptive evolution: a model
The honeybee already serves as a model organism for studying human immunity, disease resistance, allergic reaction, circadian rhythms, antibiotic resistance, the development of the brain and behavior, mental health, longevity, diseases of the X chromosome, learning and memory, as well as conditioned responses to sensory stimuli (Kohl, 2012).
My comment: The honeybee also already serves as a model organism for plasticity.
See these three publications from Anna Di Cosmo’s group for example.
Excerpt: Future work on O. vulgaris olfaction must also consider how animals acquire the odours detected by the olfactory organ and what kind of odour the olfactory organ perceives. The OL acting as control centre may be target organ for metabolic hormones such as leptin like and insulin like peptides, and olfactory organ could exert regulatory action on the OL via epigenetic effects of nutrients and pheromones on gene expression (Kohl, 2013; Elekonich and Robinson, 2000).