Subatomic: From thermophiles to humans (2)

By: James V. Kohl | Published on: February 10, 2018

Summary: As more information about natural selection for energy-dependent codon optimality made it clear that food energy was essential for species survival, the theorists continued to refuse to use experimental evidence to support their claims about how mutations and natural selection could lead to the evolution of a new species. Now, the theorists are left with foolish claims, like this “…the universe simply is, without ultimate cause or explanation.”
Why Is There Something, Rather Than Nothing? by Sean M. Carroll

…any attempt to account for the existence of something rather than nothing must ultimately bottom out in a set of brute facts; the universe simply is, without ultimate cause or explanation.

See for comparison: Evolution of Hormone-Receptor Complexity by Molecular Exploitation (co-authored by Sean M. Carroll)

…we show that, long before the hormone evolved, the receptor’s affinity for aldosterone was present as a structural by-product of its partnership with chemically similar, more ancient ligands. Introducing two amino acid changes into the ancestral sequence recapitulates the evolution of present-day receptor specificity. Our results indicate that tight interactions can evolve by molecular exploitation—recruitment of an older molecule, previously constrained for a different role, into a new functional complex.

All proximate functions linked to cell type stability and healthy longevity are energy-dependent and RNA-mediated in the context of food acquisition and the pheromone-controlled physiology of reproduction in species from microbes to humans. Questions about the fact have been answered by experimental evidence since the time that Jay R. Feierman first asked me “What about birds?” (in 1995)

His approach was different species of birds exist, which means birds evolved.

See for comparison: Avian transcriptomics: opportunities and challenges

Recent developments in next-generation sequencing technologies have greatly facilitated the study of whole transcriptomes in model and non-model species. Studying the transcriptome and how it changes across a variety of biological conditions….

Experimental proof as a last step to ascribing biological function

Experimental proof is the first step that is required to ascribe biological function. If you ask why there is something rather than nothing, you cannot just assume that the answer is unknown to serious scientists. Assumptions prevent examination of facts, which is why the claims of biologically uninformed theorists about proximate functions in astrocytes and any other claims about “proximate mechanisms” were denigrated in Dobzhansky (1964).

See: Biology, molecular and organismic

The notion has gained some currency that the only worthwhile biology is molecular biology. All else is “bird watching” or “butterfly collecting.” Bird watching and butterfly collecting are occupations manifestly unworthy of serious scientists! (p. 443)

That denigration of the works by human ethologists, theorists such as Sean M. Carroll,  and others who tout pseudoscientific nonsense was largely ignored by serious scientists. They allowed the theorists to further bastardize the claims Darwin made about “conditions of life.”

Theorists put natural selection for something besides food energy, first. As more information about natural selection for energy-dependent codon optimality made it clear that food energy was essential for species survival, the theorists continued to refuse to use experimental evidence to support their claims about how mutations and natural selection could lead to the evolution of a new species.

They collectively failed to link anything except their ridiculous theories to evolution and ignored all the facts about how food energy-dependent changes must link the sun’s anti-entropic virucidal energy to the physiology of reproduction and all biodiversity via biophysically constrained viral latency.

When you see someone, like Jay R. Feierman repeatedly make claims about “Proximate Mechanisms” that are not based on what is known about food energy and pheromone-controlled feedback loops linked to reproduction, please note:

Jay R. Feierman, who posted the nonsense about “Proximate Mechanisms” to the Human Ethology Group, has failed to examine the experimental evidence of biologically-based cause and effect for more than 50 years.

91606 Astrocyctes: Proximate Functions OPEN ACCESS

See for comparison: Dependence of RNA synthesis in isolated thymus nuclei on glycolysis, oxidative carbohydrate catabolism and a type of “oxidative phosphorylation”

The synthesis of RNA in isolated thymus nuclei is ATP dependent. Experiments are described which show that the required ATP is produced by reactions associated with glycolysis, the citric acid cycle, and a type of oxidative phosphorylation.

All that experimental evidence is missing from the representations Anthony Fitzpatrick made during this Webinar.

Untangling Neurodegenerative Diseases using Cryo-Electron Microscopy

The research focus of the Fitzpatrick Lab is to determine the structure and behavior of patient-derived amyloid fibrils and, more generally, to understand the role of protein aggregation in vivo by identifying the cellular changes that occur in response to the formation, clearance and spread of fibrillar inclusions. The methods employed by his lab are largely experimental and include cryo-electron microscopy (cryo-EM), mass spectrometry, transcriptomics, microfluidics, magic angle spinning NMR and optical super-resolution microscopy.

Anthony Fitzpatrick linked the virus-driven theft of quantized energy from hydrogen-atom transfer in DNA base pairs in solution and amino acid substitutions in microtubules to neurodegenerative diseases without mentioning what is know about the virus-driven degradation of messenger RNA, which is common to all pathology.
Use of cryo-electron microscopy (cryo-EM) outside the context of the understanding of serious scientists who have linked the sun’s anti-entropic virucidal energy to biophysically constrained viral latency and cell type stability is inappropriate.  It confuses people who may live long enough to acquire a virus-driven neurodegenerative disease.
Listen to the first 20 minutes of the free Webcast to hear him ignore that fact.
See also: Cryo-EM structures of Tau filaments from Alzheimer’s disease brain

  1. an ordered, in-register, parallel hydrogen-bonding pattern is maintained throughout the protofilament structure. Additional hydrogen bonds that stabilize the protofilament are implied by the side chains of ladders of asparagines and glutamines.
  2. A hydrophobic cluster of L324, I326 and V363 stabilizes the region immediately following the turn and the cross-β interface between β3 and β7 is further cemented by hydrogen bonds between the sidechains of H328 and T361. Following β3, residues 332PGGG335 adopt an extended β-spiral conformation.
  3. Alternating charged residues between E338 and R349 on the solvent exposed surface of the β-helix provide intramolecular charge compensation that offsets the repulsive effects of stacking sidechains with identical charge.
  4. …the glycine tripeptide adopts a characteristic polyglycine II, β-spiral structure27 that forms a hydrogen-bonding pattern both within and between the two protofilaments. The PHF interface is further stabilized by the formation of two hydrogen bonds between Q336 and the backbone carboxyl of K331 on the opposite protofilament.
  5. The β-helix in Tau is closed by G355, which is located in the 353KIGS356 motif of R4 that comprises the potential phosphorylation site S356.
  6. Knowledge of the atomic coordinates of Tau filaments may be useful for the rational design of specific inhibitors of Tau aggregation, as well as tracer compounds.

Citation: Tau proteins of Alzheimer paired helical filaments: abnormal phosphorylation of all six brain isoforms. (1992 with my emphasis)

Preparations of dispersed paired helical filaments (PHFs) from the brains of Alzheimer‘s disease and Down’s syndrome patients display on gels three principal bands corresponding to abnormally modified forms of the microtubule-associated protein tau. Interpretation of the pattern is difficult because there are six tau isoforms in normal brain and phosphorylation changes their mobility. By enzymatic dephosphorylation at high temperature, we have shifted the three abnormal bands obtained from dispersed PHFs to align with the six nonphosphorylated tau isoforms. By using antibodies specific for some of the inserts that distinguish the various isoforms and label PHFs, we have established a correspondence between PHFs, abnormal bands, and isoforms. This identification of isoforms is a necessary step in unravelling the molecular pathogenesis of PHFs.

The identification of what causes abnormally modified changes in enzymatic dephosphorylation should have linked energy-dependent changes in the fixation of RNA-mediated substitutions to the prevention of neurodegenerative diseases and all other pathology in the context of biophysically constrained viral latency and stress -linked mutations.
See for comparison: Citric acid cycle
The citric acid cycle (CAC) – also known as the tricarboxylic acid (TCA) cycle or the Krebs cycle[1][2] – is a series of chemical reactions used by all aerobic organisms to release stored energy through the oxidation of acetyl-CoA derived from carbohydrates, fats, and proteins into carbon dioxide and chemical energy in the form of adenosine triphosphate (ATP).
See also: A reversible TCA cycle in a thermophile (3)
A reversible TCA cycle in a thermophile (2)
A reversible TCA cycle in a thermophile
The overwhelming complexity of the TCA cycle is one of the first things that a creationist who is also a medical student would claim is proof of a creator God. The link from the TCA cycle in a thermophile makes it much more difficult for biologically uninformed theorists to assert their ridiculous claims.

The fact that microbial adaptation is nutrient-dependent and pheromone-controlled in thermophiles and all other microbes strikes a fatal blow to theories about mutation-driven evolution, which can now be replaced by facts that link ocean acidification from the proliferation of viruses to all pathology in species from archaea to humans via the transgenerational epigenetic inheritance of Zika virus-damaged DNA.
…microbial adaptation constitutes another possible mechanism to counteract the effects of environmental change. This idea is formulated in the coral probiotic hypothesis that posits a dynamic relationship between microorganisms and environmental conditions, which selects for the most advantageous coral holobiont13.

But wait, that was published last year.


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