Summary: To claim evolution, Koonin must link food energy from the pheromone-controlled physiology of reproduction to fixation of a beneficial mutation in the organized genome of one species that evolved into another species.
The failure to link energy-dependent base editing to RNA editing and RNA-mediated cell type differentiation in all publications about healthy longevity compared to pathology can be attributed to the pseudoscientific nonsense touted by theorists. In their ridiculous mathematical models, they claimed the emergence of energy could be linked to the evolution of all biodiversity. Their lack of experimental evidence, which is required to link biologically-based cause and effect to biodiversity, was placed into the context of “human idiocy” by Richard P. Feynman.
See Richard P. Feynman’s lecture on: Food energy. See for comparison see: Energy as information and constrained endogenous RNA interference.
Feedback loops link quantized energy as information to biophysically constrained RNA-mediated protein folding chemistry. Light induced energy-dependent changes link angstroms to ecosystems from classical physics to chemistry/chirality and to molecular epigenetics/autophagy.
The National Microbiome Initiative links microbial quorum sensing to the physiology of reproduction via endogenous RNA interference and chromosomal rearrangements. The rearrangements link energy-dependent fixed amino acid substitutions to the Precision Medicine Initiative via genome wide inferences of natural selection.
This detailed representation of energy-dependent natural selection for codon optimality links biologically- based cause and effect from G protein-coupled receptors to RNA-mediated amino acid substitutions and the functional structure of supercoiled DNA. Energy-dependent polycombic ecological adaptations are manifested in supercoiled DNA. Chromosomal inheritance links the adaptations from morphological phenotypes to healthy longevity via behavioral phenotypes. For contrast, virus-driven energy theft is the link from messenger RNA degradation to negative supercoiling, constraint breaking mutations, and hecatombic evolution. The viral hecatomb links transgenerational epigenetic inheritance from archaea to Zika virus-damaged DNA, which typically is repaired by endogenous RNA interference and fixation of RNA-mediated amino acid substitutions in organized genomes.
The failure to link energy-dependent base editing and energy-dependent RNA editing to healthy longevity predicted the failure to link the virus-driven degradation of messenger RNA to all pathology. See for instance: The Science of Personalized Nutrition
A single nucleotide polymorphism (SNP) or change occurs in nearly 1 in 1,000 base pairs and accounts for much of an individual’s uniqueness. Research on SNPs and other genetic variations like deletions, inversions, duplications and copy number variations (CNV), which represent up to 9.5 percent of the human genome, have changed the face of human nutrition and validated the concept that nutrition could and should be personalized. (Mullally, 2007)
A single nucleotide polymorphism (SNP) is a single base-pair difference in the DNA sequence of individual members of a species. SNPs in genes may lead to variations in the amino acid sequence, but SNPs can also occur in noncoding regions of DNA. Base editing of A•T to G•C in genomic DNA was linked from RNA editing to the physiology of pheromone-controlled reproduction and fixation of amino acid substitutions in organized genomes. The amino acid substitutions differentiate all cell types in all individuals of all living genera.
Bioengineer Feng Zhang of MIT’S Broad Institute notes in an email that the team employed “a comprehensive and creative approach” to achieve such precision. “As a field, we have been looking for ways to precisely rewrite parts of the genetic code,” writes Feng, whose own, CRISPR-based method to edit single bases in RNA was published today in Science. “Base editors move us closer to this goal.”
The CRISPR-based editing of single base pairs in RNA links the energy-dependent function of the innate immune system to all biophysically constrained biodiversity via the pheromone-controlled physiology of reproduction, which biophysically constrains viral latency. Natural selection for energy-dependent codon optimality, links the editing of single base pairs in RNA to every aspect of healthy longevity via RNA editing.
Reported as: RNA Editing Possible with CRISPR-Cas13
“This work is an impressive study from a highly productive research group that suggests the possibility of editing RNA transcripts to alter their coding potential in a programmable manner,” David Liu…[who] has a report out today in Nature describing specific nucleotide editing of DNA by a similar method.
Feng Zhang (base editing) gives a pat on the back to David Liu (RNA editing), and Liu reciprocated, or vice versa. Taken together, they are making face-saving attempts that ignore everything known to serious scientists about biophysically constrained viral latency.
The tool itself could be further developed, adds computational biologist Eugene Koonin of the National Center for Biotechnology Information who also was not involved in the study. “This paper is not the end of the road,” he says. It’s possible that Cas13b could be fused to a variety of editing enzymes that would allow a range of different sequence changes. The possibilities are numerous, Koonin says, and “the best is still to come.”
Koonin is a biologically uninformed science idiot who has followed in the footsteps of others like him. Their computations link mutations to evolution across millions of years. The computational biologists are evolutionary biologists who have failed to link food energy from the creation of enzymes and the the RNA-mediated editing of the enzymes, which is required to link differences in sequence changes from fixation of RNA-mediated amino acid substitutions in organized genomes to the prevention of virus-driven messenger RNA degradation. All serious scientists have linked the virus-driven degradation of messenger RNA from mutations to all pathology. Koonin’s claim that “the best is still to come” is moronic.
Every link to energy-dependent RNA-mediated cell type differentiation via the pheromone-controlled fixation of amino acid substitutions has been detailed in the context of experimental evidence. But, Koonin (2016) made this ridiculous claim:
The proper question is: how has this sequence evolved? And the proper null hypothesis posits that it is a result of neutral evolution: that is, it survives by sheer chance provided that it is not deleterious enough to be efficiently purged by purifying selection. To claim adaptation, the neutral null has to be falsified.
To claim evolution, Koonin must link food energy from the pheromone-controlled physiology of reproduction to fixation of a beneficial mutation in the organized genome of one species that evolved into another species.
If Koonin and others like him cannot provide an example of how biologically-based evolution occurs, there is only the pseudoscientific nonsense of their mathematical models for comparison to facts about: How flu shot manufacturing forces influenza to mutate
“Now we can explain — at an atomic level — why egg-based vaccine production is causing problems,” said TSRI Research Associate Nicholas Wu, Ph.D., first author of the study, published recently in the journal PLOS Pathogens.
Clearly, an explanation — at the atomic level — of how viruses adapt to the cell types of one species during the production of an egg-based vaccine must be linked from atoms to ecosystems in all living genera via adaptations in the host.
See for example: Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems (2014)
The genesis of variation is manifested in ecological variation, which confers the ability to adapt via nutrient-dependent epigenetically-effected pheromone-controlled ecological, social, neurogenic, and socio-cognitive niche construction. Niche construction is manifested in organismal complexity. Everything about ecological adaptation appears to make sense in the light of what is currently known about molecular biology. What is currently known about the conserved molecular mechanisms that link the epigenetic landscape to the physical landscape of DNA can now be compared to any forthcoming explanations that attempt to make sense of how mutation-driven evolution might occur.