Summary: RNA-guided human genome engineering presents a direct conflict to claims made in the context of CRISPR–Cas9 editing, which creates more mutations. The repair of mutations is nutrient energy-dependent and virus-driven energy theft is biophysically constrained by the physiology of pheromone-controlled reproduction. The unexpected mutations are examples of ignorance expressed by theorists in the claims about evolution. The theorists seem reluctant to admit to the facts about RNA-mediated cell type differentiation because it is energy-dependent, and most of them don’t seem to know that the quantized energy comes from sunlight.
This article became available during the last hour: Unexpected mutations after CRISPR–Cas9 editing in vivo [subscription required]
CRISPR–Cas9 editing shows promise for correcting disease-causing mutations. For example, in a recent study we used CRISPR-Cas9 for sight restoration in blind rd1 mice by correcting a mutation in the Pde6b gene1. However, concerns persist regarding secondary mutations in regions not targeted by the single guide RNA (sgRNA)2.…
It was reported as: Crack in CRISPR Façade after Unanticipated In Vivo Mutations Arise
“Researchers… may be missing potentially important mutations,” Dr. Tsang remarked. “Even a single nucleotide change can have a huge impact.”
That fact is not just a “Crack in the CRISPR Facade.” It dismisses all claims about mutation-driven evolution. Those ridiculous claims have been replaced by what is known to serious scientists about how viral latency must be biophysically constrained. It must be constrained by a light-activated endogenous substrate in all cell types of all living genera. The light comes from the sun. For example, the anti-entropic energy of ultraviolet light kills viruses.
The so called promoter-associated noncoding RNA (paRNA), microRNAs, and epigenetic regulators control transcription of the tumour suppressor E-cadherin in epithelial cancers. E-cadherin silencing is energy-dependent and RNA-mediated. The energy must link the innate immune system to an endogenous substrate, which links endogenous RNA interference to biophysically constrained protein folding chemistry via the physiology of reproduction in all living genera. These researchers report…
“…formation of a complex between the paRNA and microRNA-guided Argonaute 1 that, together, recruit SUV39H1 and induce repressive chromatin modifications in the gene promoter. A single nucleotide polymorphism (rs16260) linked to increased cancer risk alters the secondary structure of the paRNA, with the risk allele facilitating the assembly of the microRNA-guided Argonaute 1 complex and gene silencing. Collectively, these data demonstrate the role of a paRNA in E-cadherin regulation and the impact of a noncoding genetic variant on its function. Deregulation of paRNA-based epigenetic networks may contribute to cancer and other diseases making them promising targets for drug discovery.
Collectively, these researchers appear to be making a desperate attempt to keep others from leanring that everything they link to the single nucleotide polymorphism and cancer risk has already been linked by serious scientists to energy-dependent cell type differentiation and healthy longevity in all living genera via the physiology of reproduction. If they dropped their attempts to obfuscate what is known about energy-dependent biophysically constrained RNA-mediated protein folding, they would report on how virus-driven energy theft links changes in the microRNA/messenger RNA balance to all pathology.
…our data untangle the complicated roles of E-cadherin and p120 in the context of distinct junctional complexes, spatially separating their functions and providing an explanation for their conflicting behaviour in cell growth. In addition, they identify PLEKHA7 as a specific marker of ZA that mediates suppression of growth-related signalling. Finally, they reveal an interaction of the ZA with the microprocessor complex, and uncover a mechanism whereby the ZA regulates a set of miRNAs to suppress cellular transformation and maintain the epithelial phenotype.
The difference between data-based representations of biophysically constrained biologically-based cause and effect and theoretical representations that link promoter–proximal transcripts can be compared. Simply put, the theories ignore food energy as the information that sustains all RNA-mediated life on Earth. The theories invented in the published work from today substitutes what they refer to as promoter-associated RNAs, (paRNAs).
Outside the context of food energy as information, pseudoscientists claim that they do not understand how cis-acting elements in transcriptional regulation of neighbouring genes are linked to the functional structure of supercoiled DNA, which protects all orgnanized genomes from the virus-driven energy theft that links the degradation of messenger RNA from mutations to all pathology in all living genera.
See also: Discovery of extremely halophilic, methyl-reducing euryarchaea provides insights into the evolutionary origin of methanogenesis 5/30/17 by senior author Eugene Koonin
Within the phylum Euryarchaeota, these isolates form a separate, class-level lineage ‘Methanonatronarchaeia’ that is most closely related to the class Halobacteria. Similar to the Halobacteria, ‘Methanonatronarchaeia’ are extremely halophilic and do not accumulate organic osmoprotectants. The high intracellular concentration of potassium implies that ‘Methanonatronarchaeia’ employ the ‘salt-in’ osmoprotection strategy. These methanogens are heterotrophic methyl-reducers that use C1-methylated compounds as electron acceptors and formate or hydrogen as electron donors. The genomes contain an incomplete and apparently inactivated set of genes encoding the upper branch of methyl group oxidation to CO2 as well as membrane-bound heterodisulfide reductase and cytochromes. These features differentiate ‘Methanonatronarchaeia’ from all known methyl-reducing methanogens. The discovery of extremely halophilic, methyl-reducing methanogens related to haloarchaea provides insights into the origin of methanogenesis and shows that the strategies employed by methanogens to thrive in salt-saturating conditions are not limited to the classical methylotrophic pathway.
The classical methyltrophic pathway links energy-dependent changes in base pairs to RNA-directed DNA methylation and biophysically constrained changes in amino acid substitutions that are required to create the functional structure of supercoiled DNA. All the energy-dependent changes have been linked from angstroms to ecosystems in all living genera via the sense of smell in bacteria and nutrient-dependent pheromone-controlled ecological adaptations.
Eugene Koonin may have been one of the first to admit that the role of virus-driven energy theft had not been considered in the context of ridiculous claims made by neo-Darwinian theorists.
The entire evolution of the microbial world and the virus world, and the interaction between microbes and viruses and other life forms have been left out of the Modern Synthesis…
It may be fun for serious scientists to watch as he and others try to recover from their mistakes in the past by inventing new terms for use in new theories that still fail to link what serious scientists know about food energy to the physiology of reproduction and that also link virus-driven energy theft to all pathology. For example, here they do what Carl Woese did when he invented a third domain of life to fit the ridiculous theories of mutation-driven evolution. The discovery of a fourth domain, is not reported as a fourth domain. Instead moderately thermophilic and extremely halo(natrono)philic methanogens that thrive in the hypersalinity of lakes is reported to forms a class-level lineage, called ‘Methanonatronarchaeia.’ The lineage is automagically linked to the deep euryarchaeal lineage because the Methanonatronarchaeia posess a form of methlyation.
A methyl-reducing type of methanogenesis links C1-methylated compounds from their role as acceptors from formate or H2, which serve as external electron donor. This fits into the context of Darwin’s energy-dependent “conditions of life” via the transfer of quantized energy from the sun as an external electron donor to the deep euryarchaeal lineage. The difference in the electron transport mechanism supposedly also supports the claim that metabolism evolved to link their discovery to an impact on what is understood about biogeochemical cycles of protein biosynthesis and degradation, ecology and the evolution of microbial methanogenesis.
Figure 6 from this published work attests to the complexity of the “evolution of microbial methanogenesis” by placing everything into the context of energy-dependent thermodynamic cycles of RNA-mediated protein folding chemistry, which are biophysically constrained by the physiology of reproduction in species from microbes to humans.
Two complete CRISPR-Cas systems in HMET1 compared to none in AMET1 help to explain why an excess number of genes for anti-parasitic defense appear to have been created in the context of food energy-dependent lifestyle differences that indicate HMET1 is subject to much more nutrient stress and social stress due to virus-driven energy theft in the context of stronger pressure from mobile elements than AMET1.
Nothing explains why these researcher think that their ongoing obfuscation of facts about virus-driven energy theft and all pathology will continue to be acceptable to anyone who acquires and plays this cell biology game.
Cytosis: A board game taking place inside a human cell! Players compete to build enzymes, hormones and receptors and fend off attacking Viruses!