Anti-entropic containment of energy: symbiosis 1.0
Excerpt: One thing that all chemical reactions have in common—whether they are the reactions that take place inside a battery, the metabolic reactions inside a living organism, or the combustion reactions that cause an explosion—is that they all involve some kind of change in energy.
My comment: Therein lies the problem with attempts by pseudosceintists to link nutrient energy from ecological variation to epigenetically-effected ecological adaptation, which is manifested in the physical landscape of DNA in organized genomes of all genera. Unless they start with the biological energy of the sun, they must use de Vries definition of “mutation” to link atoms to ecosystems via perturbed protein folding. They try to link beneficial mutations to biodiversity, instead of linking the anti-entropic energy from the sun, which is required to support links to organism-level theromoregulation.
Organism-level thermoregulation is nutrient-energy dependent. Nutrients must be metabolized in the context of protein biosynthesis and degradation to support the physiology of reproduction and fixation of RNA-mediated amino acid substitutions in functional duplicates of RNA-mediated genes.
Schrodinger placed the sun’s biological energy into its proper perspective as the link from quantum physics to quantum biology in his 1943 lectures, which were published as his: “What is Life?” He made life more complicated for theorists who had already decided to use de Vries definition of “mutation” in their theories about how one species evolved into another.
Serious scientists have always known that doesn’t happen. They put Darwin’s ‘conditions of life’ first and view neo-Darwinian theorists in the context of those who bastardized perfectly acceptable links from observations to ideas about how differences in morphological phenotypes could arise in species that adapted to ecological variation.
In species from microbes to man, serious scientists know that adaptations are biophysically constrained by nutrient-dependent RNA-mediated protein folding chemistry, which links the epigenetic landscape to the physical landscape of DNA in organized genomes. Even among serious scientists, however, few would expect that a A single transcription factor coordinates different stress response pathways in neurons of species from nematodes to humans.
The across-species link to cell type differentiation from nematodes to humans via the conserved molecular mechanisms that link nutrient-dependent pheromone-controlled RNA-mediated cell type differentiation in species from microbes to humans may be too much for theorists to accept. But, who cares whether theorists accept facts established in the context of experimental evidence. The experimental evidence speaks to serious scientists, and they can choose to teach pseudoscientists, or not.
For example, see: Mae-Wan Ho: No Boundary Really Between Genetic and Epigenetic
…evolutionary science has now “moved on to such an extent” that she and Peter Saunders don’t really care anymore about “trying to convince the neo-Darwinists.”
The process of aging is due, in part, to protein misfolding events and a general deterioration in the quality of the proteome. In support of this hypothesis, metastable proteins that can fold and function in youthful cells begin to misfold upon aging, losing functionality (Ben-Zvi et al., 2009). A similar phenomenon appears in numerous age-onset neurodegenerative disorders, in which the aging brain can no longer maintain disease-linked proteins in properly folded, functional states and misfolding leads to multimerization of the disease proteins and neural death (Douglas and Dillin, 2010 and Morimoto, 2008). In these studies, the levels of hsf-1 and its chaperone target genes directly correlated with the age onset of different neurodegenerative models. Thus, by extension, it was hypothesized that hsf-1 regulates the aging process by modulating chaperone network components to directly influence the folding state of the proteome ( Morimoto, 2008).
My comment: Protein folding is nutrient-dependent. That’s where the energy comes from. Energy use can be view in the context of alternative splicings. They link RNA-mediated nutrient-dependent fixation of amino acids to the species-specific physiology of reproduction and chromosomal rearrangements. The chromosomal rearrangements exemplify how biologically-based cause and effect leads to the stability of organized genomes in different species. When that stability of the chromosomal rearrangements is perturbed by viruses and their replication, viral microRNAs can be linked from entropic elasticity to uncontrolled stress-related heat shock caused by the uncontrolled damage to DNA by viruses linked to pathology.
You’re not likely to see evolutionary theorists accept the fact that they missed learning about the role viruses play in perturbed protein folding. It means they also missed the role that nutrients play. Nutrients link metabolic networks to genetic networks and they quickly amplify differences in cell types of all cells in all individuals of all genera.
For example, see:
An alternative splicing event amplifies evolutionary differences between vertebrates
PTBP1 represses a network of neural-specific alternative exons in non-neural cells and tissues (8, 13, 14). Activation of this network is required for neuronal differentiation and depends on PTBP1 silencing by miR-124 (8, 13, 14). Many PTBP1-repressed exons are activated by the neuronal-specific Ser/Arg (SR)–related protein of 100 kD (nSR100/SRRM4) (15, 16).
They make no mention of the fact that the alternative splicing event is linked from ecological variation to nutrient-dependent pheromone-controlled ecological adaptations via RNA-mediated gene duplication and RNA-mediated amino acid substitutions that are fixed in the organized genomes of all genera via their physiology of reproduction. Instead, the amino acids are referred to in the context of isoforms. Few people outside the specialty area of this work would recognize the obvious link from changes in the nutrient-dependent microRNA/messenger RNA balance to the physiology of reproduction. Anyone suspicious about what appears to be an attempt to obfuscate cause and effect would find it even more difficult to unravel the events that they link from alternative splicing to cell type differentiation.
See for example:
From Wikipedia: “Serine/arginine-rich splicing factor 1 (SRSF1) also known as alternative splicing factor 1 (ASF1), pre-mRNA-splicing factor SF2 (SF2) or ASF1/SF2 is a protein that in humans is encoded by the SFRS1 gene. ASF/SF2 is an essential sequence specific splicing factor involved in pre-mRNA splicing. SFRS1 is the gene that codes for ASF/SF2 and is found on chromosome 17. The resulting splicing factor is a protein of approximately 33 kDa. ASF/SF2 is necessary for all splicing reactions to occur, and influences splice site selection in a concentration-dependent manner, resulting in alternative splicing. In addition to being involved in the splicing process, ASF/SF2 also mediates post-splicing activities, such as mRNA nuclear export and translation.”
Conclusion: Few people understand how to link quantum physics to quantum biology and nutrient-dependent RNA-mediated events to biophysically constrained protein folding, which links ecological variation to ecological adaptation in all genera via amino acid substitutions.
Few people will learn enough about cell type differentiation to ask questions about the misrepresentations made by evolutionary theorists, or those who frame their results in the context of ridiculous theories to help ensure their research will continue to be funded. The authors write:
“….mammalian-specific skipping of exon 9 modulates the splicing levels of a large number of functionally coherent PTBP1 target exons across diverse cell and tissue types.”
Alternative RNA splicing is nutrient-dependent and it links the diversity of all cell types and all tissue types in all genera from the innate immune system response to viruses to healthy longevity via DNA repair. There are no evolutionary differences; there is only ecological variation and ecological adaptation, which is nutrient-dependent and controlled by the physiology of reproduction.
See also: From Fertilization to Adult Sexual Behavior
Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to sexual differentiation in at least two species, Drosophila melanogaster and Caenorhabditis elegans (Adler and Hajduk, 1994; de Bono, Zarkower, and Hodgkin, 1995; Ge, Zuo, and Manley, 1991; Green, 1991; Parkhurst and Meneely, 1994; Wilkins, 1995; Wolfner, 1988). That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes.
My comment: Alternative RNA splicing links ecological variation to nutrient-dependent ecological adaptation. Ecologists know the difference between evolution and ecological speciation. When more serious scientists learn about ecological speciation fewer will be forced to write about evolution.
But, for now, see:
Alternative RNA Splicing in Evolution
…alternative splicing may be the critical source of evolutionary changes differentiating primates and humans from other creatures such as worms and flies with a similar number of genes.