Biophysically constrained fast adaptations (2)
(click to enlarge)Carl Zimmer made a podcast. There are eight episodes of “What Is Life?” He asks people who he thinks are experts about the big question. They fail to explain how the creation of energy must biophysically constrain viral latency.
On March 30, 2016, the question became What is life when it is not protected from virus driven entropy? (video) The answer was based on what all serious scientists know about the creation of energy and microRNA biogenesis, ATP, RNA et al. See: Energy as information and constrained endogenous RNA interference (video)
See also: Causation, constructors and codes (February, 2018)
A formal definition of codes in general, and organic codes in particular, allows the relational diagram to be extended so as to capture this translation of formal cause into process. The extended relational diagram is used to exemplify causal entailment in a diverse range of processes, such as enzyme action, construction of automata, communication through the Morse code, and ribosomal polypeptide synthesis through the genetic code.
One year later and we see that the Institute for Creation Research science ministry and most science journalists are in trouble. Their researchers and sources failed to realize that natural selection for energy-dependent codon optimality biophysically constrains viral latency via amino acid substitutions that repair DNA and differentiate all cell types in all individuals of all living genera.
Codon identity regulates mRNA stability and translation efficiency during the maternal-to-zygotic transition
The amino acid optimality code (Fig 6) provides an alternative perspective on sequence changes between paralogs in evolution and human disease.
This code integrates integrates the creation of ATP and RNA with multiple inputs of energy-dependent translation to peptide bond formation, amino acid identity, and other factors influencing the translocation rate across cellular transitions, tissues, and pathological states.
When the cure for cancer was announced, it linked the creation of energy to light-activated microRNA biogenesis and the creation of ATP and RNA to the energy-dependent creation of base pairs, peptide bond formation, amino acid identity, and biophysically constrained viral latency. That is exemplified in the mouse-to-human model of pheromone-controlled reproduction and the EDAR V370A variant.
Nutrient-dependent Pheromone-Controlled Ecological Adaptations: From Angstroms to Ecosystems
See also: A cure for cancer? Israeli scientists say they think they found one
The potentially game-changing anti-cancer drug is based on SoAP technology, which belongs to the phage display group of technologies. It involves the introduction of DNA coding for a protein, such as an antibody, into a bacteriophage – a virus that infects bacteria. That protein is then displayed on the surface of the phage. Researchers can use these protein-displaying phages to screen for interactions with other proteins, DNA sequences and small molecules.
In 2018, a team of scientists won the Nobel Prize for their work on phage display in the directed evolution of new proteins – in particular, for the production of antibody therapeutics.
AEBi is doing something similar but with peptides, compounds of two or more amino acids linked in a chain. According to Morad, peptides have several advantages over antibodies, including that they are smaller, cheaper, and easier to produce and regulate.
The peptides do not create themselves. Listen for the claim that every angstrom is dynamic. See:
See for comparison: Leveraging Single-Cell Genomics to Identify Drivers of Enhanced Immunity (1/31/19)
My summary: Alex K. Shalek discussed single-cell genomic approaches and his exploration of the functional diversity of creation. Every aspect of cell type creation occurs only in the context of energy-dependent microRNA-mediated biophysically constrained immune cells within and across individuals.
Before the webinar started, I asked: Is publication of “A self-assembled peptide nucleic acid-microRNA nanocomplex for dual modulation of cancer-related microRNAs” relevant to enhanced immunity?”
My question was ignored. Thankfully, the answer is obvious. Assembly of the energy-dependent peptide-nucleic acid-microRNA nanocomplex requires the link from the creation of the sun’s energy to the energy-dependent creation of base pairs and supercoiled DNA. The facts about the creation of supercoiled DNA require a link from light-activated microRNA biogenesis in plants to biophysically constrained viral latency.
See for instance: Structural diversity of supercoiled DNA
Six decades after the elucidation of its double helical structure, DNA continues to surprise us by revealing new information. Our cryo-ET, biochemical, and computational studies show the astounding versatility and dynamism of DNA depending on the degree of supercoiling. DNA simultaneously exists in a largely inactive B-form with bases tucked in and protected and an active, highly varied structure with exposed bases. Our data provide relative comparisons of supercoiling-dependent twisted, writhed, curved, and kinked conformations and associated base exposure. Each of these structural features may be differentially recognized by the proteins, nucleic acids, and small molecules that modulate DNA metabolic processes.
MicroRNAs are the small molecules that modulate DNA metabolic processes. All the facts have been detailed by serious scientists. Even when they do not explicitly state that they are starting from the creation of the sun’s anti-entropic virucidal energy, other serious scientists know that they are. No serious scientist starts with the emergence of energy and links it from mutations to evolution.
But let’s not forget the “alternative facts” about what causes cancer.
For example, see:
‘Bad luck’ of random mutations plays predominant role in cancer, study shows (1/1/15)
…two-thirds of adult cancer incidence across tissues can be explained primarily by “bad luck,” when these random mutations occur in genes that can drive cancer growth, while the remaining third are due to environmental factors and inherited genes.
See also:Enhancer hijacking activates oncogenic transcription factor NR4A3 in acinic cell carcinomas of the salivary glands (1/21/19)
Reported as: Genetic causes of tumors in salivary glands (1/31/19)
The virus-driven degradation of messenger RNA causes the “switch” to stay on. They refer to this as “enhancer hijacking” to obfuscate the facts, so you are less likely to link biophysically constrained chromosomal rearrangements to sympatric speciation.
But see: What makes two species different?
…sex chromosomes evolve to be genetically incompatible between species faster than the rest of the genetic chromosomes and reveal the factors at play in this incompatibility.
The electron transport chain (ETC), the centre for ATP production, is composed of 13 mtDNA-coded proteins and 73 nDNA-coded proteins. Here we use an expanded sequence-capture genomic sequence dataset from 96 individuals of the same and additional populations to validate previous findings that the ecotypes have unique mtDNA haplotypes with two amino acid changes in ND5 and CYTB that are highly segregated between ecotypes. This striking population structure at the mtDNA is in contrast to the low genetic structure seen in the background nDNA. We now incorporate analyses from the nDNA-coded ETC genes, comparing several bioinformatics approaches for sequence assembly and extraction of SNP data. Contrasts between the variation in mtDNA-coded and nDNA-coded ETC genes are made at the level of the gene, protein, and ETC complex and interpreted in the context of mitochondrial physiology and function.
The divergence among vertebrates is not due to selfish gene flow and the evolution of sex chromosomes. It is due to the creation of energy in the context of the light-activated electron transport chain and the pheromone-controlled physiology of reproduction in species from microbes to humans. Viral latency must be biophysically constrained by fixation of amino acid substitutions in organized genomes.
