Summary: Food energy-dependent base editing has been linked to biophysically constrained viral latency via microRNA editing, RNA editing and the pheromone-controlled fixation of RNA-mediated amino acid substitutions in species from microbes to humans.

Correction of β-thalassemia mutant by base editor in human embryos


Intriguingly, we found that HBB −28 (A>G) mutation repairing efficiency was about 20% in the constructed cell line and primary skin fibroblast cells. Although 10.7% of the repaired skin fibroblast cells were heterozygous, it is still able to cure anemia (Dever et al., 2016). Whether base editors will be equally or more efficient in human hematopoietic stem cells is still under investigation. High repairing efficiency in human hematopoietic stem cells will lead to new therapeutics for β-thalassemia intermedia and β-thalassemia major patients with HBB −28 (A>G) mutation.

Reported as: Challenging Darwin: an ‘evolution machine’ for biomolecules

…genetically engineered phages infect different bacterial strains under selective stimuli, such as different growth conditions, and they respond and adapt to each change artificially introduced in the environment.

The food energy-dependent base editing has been linked to biophysically constrained viral latency via microRNA editing, RNA editing and the pheromone-controlled fixation of RNA-mediated amino acid substitutions in species from microbes to humans.

See for comparison: Molecular diversity through RNA editing: a balancing act

Alteration of amino acid codons, splice patterns, stability or localization of protein-coding transcripts, modulation of regulatory RNA biogenesis and function, as well as crosstalk of RNA editing with RNA processing and silencing pathways provides a rich resource for the generation of molecular diversity and for gene regulation. These findings also illustrate that we are only beginning to understand how RNA editing is integrated into the biological networks of gene expression, regulatory pathways and genome evolution.

All claims about “genome evolution” were based on mathematical models of how mutations might lead from natural selection the creation of new species. No serious scientists believed those claims. Feynman placed them into the context of “human idiocy.”


See also my comment to the Human Ethology Yahoo Group: My comment was divorced from the announcement of the article as Fwd: U. Warwick 2017 [ Challenging Darwin: an ‘evolution machine’ for biomolecules ]

Excerpt: “A new device produces desirable molecules by modifying the environments where virus and bacteria interact”

My comment: They are not challenging Darwin, whose “conditions of life” required the link from food odors to pheromone-controlled viral latency. They are challenging the neo-Darwinian pseudoscientific nonsense that linked the virus-driven degradation of messenger RNA from mutations to evolution, which was the most ignorant explanation of biologically-based cause and effect to ever reach acceptance among the suffering masses who have continued to suffer unnecessarily and die prematurely from the virus-driven theft of quantized energy as information that is required for survival of all species.

Conserved microRNA editing in mammalian evolution, development and disease

miRNAs are greatly overrepresented among conserved editing targets.

The claims about evolutionarily conserved site-specific microRNA (miRNA) editing and the diversity the increased functional diversity of mammalian miRNA transcriptomes do not link the anti-entropic virucidal energy of the sun from microRNA editing to claims about the integral and evolutionarily stable feature of mammalian transcriptomes.

See for comparison: RNA editing independently occurs at three mir-376a-1 sites and may compromise the stability of the microRNA hairpin

RNA editing is being recognized as an important post-transcriptional mechanism that may have crucial roles in introducing genetic variation and phenotypic diversity. Despite microRNA editing recurrence, defining its biological relevance is still under extended debate. To better understand microRNA editing function and regulation we performed an exhaustive characterization of the A-to-I site-specific patterns in mir-376a-1, a mammalian microRNA which RNA editing is involved in the regulation of development and in disease. Thorough an integrative approach based on high-throughput small RNA sequencing, Sanger sequencing and computer simulations we explored mir-376a-1 editing in samples from various individuals and primate species including human placenta and macaque, gorilla, chimpanzee and human brain cortex. We observed that mir-376a-1 editing is a common phenomenon in the mature and primary microRNA molecules and it is more frequently detected in brain than in placenta. Primary mir-376a-1 is edited at three positions, -1, +4 and +44. Editing frequency estimations and in silico simulations indicated that editing was not equally recurrent along the three mir-376a-1 sites, nevertheless no epistatic interactions among them were observed. Particularly, the +4 site, located in the seed region of the mature miR-376a-5p, reached the highest editing frequency in all samples. Secondary structure predictions revealed that the +4 position was the one that conferred the highest stability to the mir-376a-1 hairpin. We suggest that molecular stability might partially explain the editing recurrence observed in certain microRNAs and that editing events conferring new functional regulatory roles in particular tissues and species could have been conserved along evolution, as it might be the case of mir-376a-1 in primate brain cortex.



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