Most consider viruses to be a legion of cripples, sterilised by ultraviolet radiation and rendered impotent by hosts that are largely immune to their threat. But a few researchers take the opposite view. And if they turn out to be right, viruses could radically alter the balance of life in the oceans, ripping away huge parts of the food web that supports whales, sea birds and the fisheries on which many people rely.
See the discussion attempt at: What does DNA have to do with the Origin of Life ?
My comment: Supercoiled DNA is the link from energy-dependent changes in angstroms to all ecosystems in all living genera. That fact has been established in the context of experimental evidence that links physics and chemistry to molecular epigenetics and biophysically constrained RNA-mediated cell type differentiation at the level of quantum consciousness.
In an attempt to discuss my model on a Facebook group where Larry Kinser Jr., is an administrator and Taylor Kessinger is an antagonist,
I wrote: I predict that this group will be the first to link virus-driven energy theft to negative supercoiling in bacteria, but a student from Susan Rosenberg’s lab was on the same track several months ago when she contacted me. I also predict that mathematical models will continue to be as useless as they always have been due to their lack of explanatory power.
Previously, co-author Angelica Parente wrote: Do you have a source on this? I study bacterial supercoiling in the context of topoisomerase II structural biology. I’m assuming in honeybees it’s affecting chromatin dynamics? My lab would be really interested in learning more about this.
See also: Asking the right questions (1)
My comment: The Journal of Molecular Biology topic is “Mechanisms and Functional Diversity of Macromolecular Remodeling by ATP-Dependent Motors.” The authors have linked energy-dependent changes from angstroms to ecosystems via the conserved molecular mechanism of autophagy. The mechanisms link the innate immune system of bacteria to their nutrient-dependent pheromone-controlled physiology of reproduction, which biophysically constrains virus-driven energy theft and all pathology in all living genera.
1) Larry Kisner Sr. If the sun could kill viruses, you could harness that and win the nobel prizw
2) Larry Kisner Sr. there is no alternate model
3) Larry Kisner Sr. Evolution must be bottom-up
Summary: The anti-entropic energy of virucidal ultraviolet light kills viruses. I have linked that fact from top-down energy-dependent causation in a model that links nutrient-dependent pheromone-controlled biophysically constrained RNA-mediated protein folding chemistry from amino acid substitutions in supercoiled DNA to protection of organized genomes from virus-driven entropy, which is the cause of all pathology.
Although Larry Kinser Sr. did not know that sunlight could kill viruses, he has since learned how I linked that fact to polycombic ecological adaptations in all living genera, and is closing fast on my claims that hecatombic evolution is the cause of all pathology. If he is motivated by money, he will present the facts I have detailed as if they were his own ideas. Others have been doing that for more than 20 years, but it is especially frustrating when other people who are supposedly young earth creationists do it.
Is someone pretending to be Larry Kinser Sr., the administrator of a “false flag” group [The Battlefield]? I will not know until he either bans me from participation in the group, or admits that he is merely using my detailed model to convince others about the facts of Creation science so that they can dismiss the claims of biologically uniformed theorists.
Until then, Taylor Kessinger, or someone pretending to be Taylor Kessinger, claims to have a model that can be compared to mine.
He is the co-author of Coalescence and genetic diversity in sexual populations under selection
Our model provides the background on top of which such singular adaptations can be sought, and understanding the statistical patterns of diversity and linkage within this null model is essential for reliable inference.
My comment: Anyone who thinks that this is a model of biologically-based cause and effect need only read the concluding sentence. It is nothing more than a theory of unreliable inferences. There is no claim about what must be selected to get from unicelluar to multicellular organisms or to sex differences in the cell types of yeasts. It is a mathematical model with no explanatory power.
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’
Characterization of Genetic Diversity in the Nematode Pristionchus pacificus from Population-Scale Resequencing Data is listed as one of the other papers that cited the paper co-authored by Taylor Kessinger. The paper that Kessinger co-authored was not cited.
If it had been cited, Kessinger could be taken to task for not knowing how his mathematical model must be linked from the nutrient-dependent pheromone-controlled physiology of reproduction in C. elegans to the morphological and behavioral diversity of the predatory nematode P. pacificus.
Instead of his inference of evolutionary history and charaterization of “…coalescence, genetic diversity, and the speed of adaptation in the infinitesimal model of quantitative genetics.” Taylor Kessinger would have a model for comparison to mine.
The two models could then be compared to representations in Natural selection constrains neutral diversity across a wide range of species to show that natural selection for energy-dependent codon optimality is nutrient-dependent.
…natural selection constrains levels of neutral genetic diversity across many species. This implies that natural selection may provide an explanation for this longstanding paradox of population genetics.
Kessinger may think that he has characterized an evolutionary history of “…coalescence, genetic diversity, and the speed of adaptation in the infinitesimal model of quantitative genetics.” Instead he has merely inferred the evolutionary history that prevents others from comparing ridiculous theories based on population genetics in the context of results like these:
“By studying the genomes of these parasites we found two genetic markers that are linked with piperaquine resistance. Not only can we now use these markers to monitor the spread of the drug resistant malaria, they will also help towards understanding as much as possible about the biology and evolution of the parasite.”
Journal article excerpt:
The first marker is a [base pair change. It is referred to as a] single-nucleotide polymorphism, which encodes a glutamic acid-to-glycine aminoacid substitution, in a putative exonuclease gene. This exonuclease marker is associated… a low rate (0·38) of dihydroartemisinin–piperaquine treatment efficacy… in Cambodia but not in other areas of the world…. The second marker is… a strong candidate for causal mutation because plasmepsins encode aspartic proteases, which are involved in the parasite’s haemoglobin degradation pathway…
Summary: Energy-dependent base pair changes and amino acid substitutions in the exonuclease gene are linked to the stability of supercoiled DNA. In all living genera the stability of supercoiled DNA is nutrient-dependent and pheromone-controlled via the physiology of reproduction. Here, the energy-dependent base pair change and RNA-mediated amino acid substitutions are found with the plasmepsin markers, and the aspartic proteases, which should be linked from energy-dependent changes in the microRNA/messenger RNA balance and mRNA degradation. The mRNA degradation links virus-driven energy theft to kelch13 gene mutations and a single copy of the mdr1 gene, which is associated with cell type differentiation in mosquitoes with decreased piperaquine, but increased mefloquine, susceptibility.
Because these researchers failed to start with energy-dependent changes in hydrogen-atom transfer in DNA base pairs in solution they missed every other step that links nutrient energy-dependent base pair changes to healthy longevity. They also missed every other step that links virus-driven energy-dependent from the loss of quantised energy and loss of information as energy from virus-driven energy theft to all pathology.
If the researchers knew anything about energy-dependent autophagy, they could link nutrient energy-dependent base pair changes to healthy longevity in the populations of different regions via the amino acid substitutions and link virus-driven energy theft to the mutations, which are linked to all pathology in all living genera.
Instead, we have yet another example of how people are being killed by neo-Darwinian theories that link mutations to pathology and to the evolution of new species via natural selection.
See also: Why bad genes aren’t always bad news
“We don’t really understand why some people with damaging mutations get the disease and some don’t. Some of this could be due to environment, but a lot of could be due to the presence of other mutations that are suppressing the effects of the first mutation,” said Roth, who is also a Senior Scientist at Sinai Health System’s Lunenfeld-Tanenbaum Research Institute.
Imagine being stuck in a room with a broken thermostat and it’s getting too hot. To cool down, you could fix the thermostat—or you could just break a window. This is how genetic suppression works to keep cells healthy despite damaging mutations. And it opens a new way of understanding, and maybe even treating, genetic disorders.
“We’ve uncovered fundamental principles of genetic suppression and show that damaging mutations and their suppressors are generally found in genes that are functionally related. Instead of looking for a needle in the haystack, we can now narrow down our focus when searching for suppressors of genetic disorders in humans. We’ve gone from a search area spanning 20,000 genes to hundreds, or even dozens. That’s a big step forward,” said Boone.
My comment: Researchers like this have never made a big step forward, and they probably never will. They obviously do not know enough about energy-dependent RNA-mediated cell type differentiation to link it from virus-driven energy theft and all pathology by as little as one base pair change and one amino acid substitution.