The tendency of the spectral redshift of glutamate-induced biophotonic emissions in this study is in the order of frog, mouse, chicken, pig, monkey, and human, which is almost consistent with the phylogenetic tree. Although the present imaging technique could not distinguish and determine what types of neurons emit what types of spectral biophotons or whether a neuron or type of neurons emit different spectral biophotons, we indeed observed the evolutionary conservation in glutamate-induced biophotonic emissions in the near-blue spectra (λmin) from chicken to pig to monkey to human (Fig. 3 F and H).
Researchers at the Wuhan Institute of Neuroscience and Neuro-engineering have previously carried out studies backing the theory that the brain not only processes and passes on information not only through electrical and chemical signals, but also with photons of light.
There is a model that links biophotonic energy as information to electrical and chemical signaling to increasing organismal complexity in all living genera. The model also links virus-driven energy theft to all pathology. See: RNA-mediated physics, chemistry, and molecular epigenetics
RNA-mediated protein folding chemistry and amino acid substitutions link the anti-entropic quantized energy of sunlight from the virucidal effects of ultraviolet (UV) light to healthy longevity via biophysically-constrained energy-dependent hydrogen-atom transfer in DNA base pairs in solution and cell type differentiation.
This question must be asked: Is quantum relativity irrelevant to theoretical physicists and neo-Darwinian theorists? The answer must be placed into the context of what is known to serious scientists about cell type differentiation. Serious scientists do not frame their results or their explanations in the context of neo-Darwinian nonsense about de novo mutations.
We present a six year old, nonverbal African American female with microcephaly, autism, global developmental delay, and metopic craniosynostosis. Exome sequencing of the patient and her two parents revealed a heterozygous two base pair de novo deletion, c.1897_1898delCA, p.Gln633ValfsX13 in ASXL3, predicted to result in a frameshift at codon 633 with substitution of a valine for a glutamine and introduction of a premature stop codon.
I asked a co-author of De novo frameshift mutation in ASXL3 in a patient with global developmental delay, microcephaly, and craniofacial anomalies two questions to determine what prevents the de novo frameshift mutation? Simply put, what prevents the pathology that she attributed to a de novo mutation?
See: Pediatric genetics – Applications of NGS in the Clinic (May 11, 2016)
I asked if the Zika virus could cause a de novo frameshift mutation. My question about the Zika virus is at 48:36
In my model, quantized energy prevents de novo mutations via energy-dependent changes in hydrogen-atom transfer in DNA base pairs in solution that link codon usage from RNA-mediated protein folding chemistry from amino acid substitutions to supercoiled DNA. Mutation and amino acid substitution are not used interchangeably. That helps to explain why I do not believe that random mutations can be linked from natural selection to the stability of organized genomes, which is required to prevent virus-driven entropy. Emily Farrow’s answer left out everything known to all serious scientists about the links from energy-dependent changes in atoms to ecosystems. She claimed that viruses are known to mutate themselves, and indicated the effect was not due to changes in base pairs.
My follow-up question is at 53:58
Do you teach students how to differentiate between mutations and amino acid substitutions?
Emily Farrow claimed that: “…we use those terms interchangeably.” She added that sometimes the change in DNA can cause a change in the amino acid, and may have confused others with her claim that all variants are mutations but not all mutations result in amino acid changes.
See for comparison: Epigenetics and Genetics of Viral Latency
… viral latency is responsible for life-long pathogenesis and mortality risk…
It should be obvious that ecological variation must link viral persistence to viral latency, which prevents virus-driven energy theft from causing the base pair changes that have been consistently linked either to energy-dependent healthy longevity or from virus-driven energy theft to all pathology. Simply put, natural selection for codon usage must link RNA-mediated protein folding chemistry to biophysically constrained fixation of RNA-mediated amino acid substitutions that stabilize the supercoiled DNA of all living genera.
…mutation in miRNAs is tightly constrained by fidelity to miRNA binding sites in target transcripts .
Reported as: ‘Junk DNA’ Used To Sort Species
Non-coding RNAs such as microRNAs (miRNA) are now recognized as important regulators of gene expression. Now, a team of researchers led by Professor Jerome Hui from the Chinese University of Hong Kong has found another use for miRNA—to understand the evolutionary relationship between different species. They first compared non-coding sequences between human, chimpanzee, gorilla, orangutan, and macaque, and successfully recovered the evolutionary history of human and our close relative, showing that chimpanzees share the closest common ancestor with human, followed by gorilla, orangutan, and then macaque being the more distant relatives. They have also successfully used this new method to reveal the relationships of other animals, such as the insects and nematodes. “Everyone in the field seems to be focusing on the meaningful microRNAs themselves, and did not pay too much attention to other ‘junk’. So this discovery is fortunate. Certainly the utilization of these regions to resolve relationships as a new method is just the beginning,” Hui said. “Understanding how they function is of extreme importance from fundamentally discover how the nature of these “dark matter”, which can potentially be useful from increasing aqua- or agricultural productions, combating pests, to diseases treatment.”
Mutation in microRNA is tightly constrained by energy-dependent links from nutritional epigenetics to cell type differentiation, which are RNA-mediated in species from microbes to humans.
In summary, using a new IL-21eGFP reporter mouse strain we identified a subpopulation of highly differentiated T helper cells in PP of the gutthat are induced by intestinal bacteria and regulate GC and IgG1 responses in PP. We have thus generated an experimental system that can facilitate the identification of the specific antigenic determinants, cellular interactions and environmental factors involved in the induction of highly differentiated intestinal Tfh cells. This can lead to a better understanding of the homeostatic relationships between the adaptive immune system and the indigenous intestinal bacteria.
For comparison, see: Producing Many Kinds of T Helper Cells by Jon Lieff
This entry was posted in Blog, Cellular Intelligence and tagged Mannose and fucose on microbes determine differentiation of T cells, Special receptors on dendritic cells determine differentiation of T helper cells, T help cells respond to carbohydrates on microbes.
Communication between subsets of dendritic cells and the many T cells is much more complex than previously understood. Elaborate signaling of T cells is just beginning to be understood.
This atoms to ecosystems model of ecological adaptations links nutrient-dependent epigenetic effects on base pairs and amino acid substitutions to pheromone-controlled changes in the microRNA / messenger RNA balance and chromosomal rearrangements. The nutrient-dependent pheromone-controlled changes are required for the thermodynamic regulation of intracellular signaling, which enables biophysically constrained nutrient-dependent protein folding; experience-dependent receptor-mediated behaviors, and organism-level thermoregulation in ever-changing ecological niches and social niches. Nutrient-dependent pheromone-controlled ecological, social, neurogenic and socio-cognitive niche construction are manifested in increasing organismal complexity in species from microbes to man.
Jon Lieff is one of the most intelligent theorists I have encountered, but he still presents neo-Darwinian pseudoscientific nonsense as if it had not all be refuted by experimental evidence that links the complexity of molecular epigenetics to energy-dependent codon usage. Codon usage and RNA-mediated protein folding chemistry link were included in this published work from 2005: Feedback loops link odor and pheromone signaling with reproduction
These results may reflect a strategy wherein GnRH neurons can modify diverse functions in order to coordinate the internal state of the animal and its behavior with reproduction in order to optimize reproductive success.
Results from a decade ago link natural selection of what to eat to the physiology of reproduction in gut bacteria and our nutrient-dependent pheromone-controlled physiology of reproduction. Results from a decade ago also link what is known about the energy-dependent physiology of reproduction in all invertebrates to all vertebrates.
Future work on O. vulgaris olfaction must also consider how animals acquire the odours detected by the olfactory organ and what kind of odour the olfactory organ perceives. The OL acting as control centre may be target organ for metabolic hormones such as leptin like and insulin like peptides, and olfactory organ could exert regulatory action on the OL via epigenetic effects of nutrients and pheromones on gene expression (Kohl, 2013; Elekonich and Robinson, 2000).
Future works that do not link energy-dependent changes from codon usage to RNA-mediated protein folding chemistry and biophysically constrained cell type differentiation by what is known about how virus-driven energy theft is linked to all pathology should be considered only as examples of pseudoscientific nonsense touted by theorists. The examples can be compared to the works of serious scientists as they continue to link energy-dependent changes from angstroms to ecosystems in all living genera.
PuMa Tse at Quantum Relativity removed several of my posts to his group after I established the fact that Lenski’s claims about mutations and evolution had been refuted in their entirety. Here’s another summary, some of which paraphrases a report by Casey Luskin.
One line of evidence derives from the expectation that synonymous substitutions—point mutations in protein-coding genes that do not affect the amino-acid sequence—are neutral and should therefore accumulate at a rate equal to the underlying mutation rate20,35. This expectation is not strictly true owing to selection on codon usage, RNA folding, and other effects, but it is generally thought that such selection is extremely weak, affects only a small fraction of sites at risk for synonymous mutations, or both 36,37.