Ricki Lewis’ Time Machine (3)

By: James V. Kohl | Published on: March 27, 2016

See also:

Ricki Lewis’ Time Machine

Ricki Lewis Time Machine (2)

DNA video in real time. Show the amazing process of DNA transcription using amino acids to turn genes into proteins.

My comment: The amino acids are nutrient-dependent and linked to supercoiled DNA by energy-dependent changes in the innate immune system. The innate immune system links metabolic networks and genetic networks to supercoiled DNA. The fact that the amino acid substitutions link the innate immune system to all biodiversity in all individuals of all living genera is a problem that Venter’s group just realized may be insurmountable.

Craig Venter’s Synthetic Genome 3.0 Evokes Classic Experiments


Of course without a time machine we can’t ever truly know how life on Earth began, and that’s why Dr. Venter stressed the importance of the word “a” before “minimal bacterial genome” in the paper’s title.

My comment: The “minimal bacterial genome” contains genes that contribute 31.5% of what is not known about cell type structure and function, despite all attempts to link glucose uptake in controlled conditions to differences in cell types.

See also:

A Challenge to the Supremacy of DNA as the Genetic Material


One sentence from the news release grabbed me: “The result is evolution from simpler to more complex and diverse organisms in both form and function, without the need to invoke genes.” Instead, Drs. Annila and Baverstock invoke thermodynamics.

I presented this in 2013: Nutrient-dependent / Pheromone-controlled thermodynamics and thermoregulation
Abstract: Natural selection for nutrients results in their metabolism to pheromones that control reproduction in species from microbes to man. In some species, sex differences in pheromones enable sexual selection. Using what is known about the molecular mechanisms common to species from microbes to man, an argument can be made from biological facts that extends to non-random nutrient-dependent pheromone-controlled adaptive evolution. This biological-based argument can be compared to arguments that might be made to support a cosmological / mathematical argument for random mutations theory.

Comments on the article by Ricki Lewis include:

“Attributing cause and effect to microbes that have somehow mutated and become resistant to antibiotics is pseudoscientific nonsense.”
Well, I think trying to explain all resistence and adaptation with no recourse to mutation is pseudoscientific nonsense too. Anyway, as long your work provides new insight, regardless of what survives later on, I’m all for it.

My comment: Two years ago, Pedro made it clear that others probably would not accept the fact that examples of hydrogen-atom transfer in DNA base pairs in solution begin with the link from the virucidal epigenetic effect of UV light. My insight linked what Ricki Lewis learned from Greg Bear about viruses to what Greg Bear incorporated into his novels on pheromones and the creation of a new human subspecies.
See:  Can a Quirky Chromosome Create a Second Human Species?
Excerpt 1):

The possibility of a new human species with 44 chromosomes can flesh out science fiction plots, if different sets of mutations accumulate in the two populations derived from the ancestral one. It may explain the origin of the bluish ghoulish subterranean Morlocks who eat the sun-loving, peaceful aboveground Eloi in H.G. Wells’ future world of The Time Machine, written in 1898.

Excerpt 2)

Neither H. G. Wells nor Wayward Pines’ creator Blake Crouch evoked Robertsonian translocation as a plausible route to rapid human evolution (or devolution) — but they could have. Sci-fi author Greg Bear came very close in his marvelous 1999 and 2003 novels Darwin’s Radio and Darwin’s Children. He imagines that a latent retrovirus awakened in the genomes of pregnant women in 1999 shuffled the genomes of a new generation in ways that created cells with 52 chromosomes instead of 46, thereby instantly establishing a group that can successfully mate only among themselves. You’ll have to read the books to learn how and why the “virus children” are superior.
Food odors link quantum physics from hydrogen-atom transfer in DNA base pairs to the nutrient-dependent de novo creation of olfactory receptor genes. Stress-linked unrepaired DNA damage leads to loss of function in genes. Loss of function is linked to the creation of olfactory receptor pseudogenes. Stress-linked loss of function links less diversity in our diet to less de novo gene creation and to the loss of genes that link the number of chromosomes in other species [48 in chimps] to 46 in humans.

See also: Difficulties of the Theory of Descent with Modification

…if my theory be true, numberless intermediate varieties, linking closely together all the species of the same group, must assuredly have existed; but the very process of natural selection constantly tends, as has been so often remarked, to exterminate the parent-forms and the intermediate links. Consequently evidence of their former existence could be found only amongst fossil remains, which are preserved, as we shall attempt to show in a future chapter, in an extremely imperfect and intermittent record.

My comment:  Venter’s group seems to have run into a common problem with attempts to explain nutrient-dependent RNA-mediated cell type differentiation. Descent with modification is attributed to gene loss not the creation of new genes. They use mutagenesis to strip the genome to its minimum where they think it could be altered by evolution, which leads them to use terms like mutation instead of amino acid substitution. De novo gene creation, the “holy grail” of biology is nutrient-dependent RNA-mediated and linked by amino acid substitutions from microRNAs to adhesion proteins and supercoiled DNA, which protects organized genomes from virus-driven energy theft and entropy.

See their references for this link to work on viruses: Synthetic generation of influenza vaccine viruses for rapid response to pandemics. It should have led Venter to recognize that virus-driven pathology can be linked from a single amino acid substitution in the influenza virus to all pathology. See: Substitutions Near the Receptor Binding Site Determine Major Antigenic Change During Influenza Virus Evolution. The authors admitted: The major antigenic changes of the influenza virus are primarily caused by a single amino acid near the receptor binding site.

Unfortunately, Venter’s group doesn’t seem to recognize the role that the innate immune system plays in preventing pathology. It pits nutrient-dependent RNA-mediated amino acid substitutions against the viruses during thermodynamic cycles of protein biosynthesis and degradation that link life history transitions in behavior to morphological and behavioral phenotypes and all biodiversity. Obviously, the difference between the amino acid substitutions and the mutations is that the substitutions are biophysically constrained. Unfortunately, some people may have been confused by Dobzhansky’s joke about the “light of evolution.”
Dobzhansky (1973) used “amino acid” and “mutation” in the context of claims that we know can be supported only with experimental evidence that links atoms to ecosystems in all living genera via the physiology of reproduction. The nutrient-dependent physiology of reproduction is biophysically constrained by the innate immune system, which is the RNA-mediated link to supercoiled DNA. Supercoiled DNA protects all organized genomes from virus-driven entropy.
If I had Ricki Lewis’ “time machine” and wanted to again learn the functions of 31.5% of the genes that aren’t known to Venter’s group, I would start from the beginning by introducing viruses into the cell and pray that the synthetic life I created would not kill us all before someone else learned how virus-driven entropy has been biophysically constrained by virucidal UV light and hydrogen-atom transfer in DNA base pairs in solution from the dawn of creation.
See also: Perez J (2015) Deciphering Hidden DNA Meta-Codes -The Great Unification & Master Code of Biology. J Glycomics Lipidomics 5:131.

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