Model vs theory: Progress report!
On June 14, 2013,
1) Nutrient-dependent/pheromone-controlled adaptive evolution: a model and
2) Mutation-Driven Evolution
were published with divergent/opposite conclusions.
1) …the largest contributor to the development of our personal preferences may be the unconscious epigenetic effects of food odors and pheromones on hormones that organize and activate behavior. If so, the model represented here is consistent with what is known about the epigenetic effects of ecologically important nutrients and pheromones on the adaptively evolved behavior of species from microbes to man. Minimally, this model can be compared to any other factual representations of epigenesis and epistasis for determination of the best scientific ‘fit’.
2) …genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world. In this view of evolution there is no need of considering teleological elements.
Since June 14, 2013, no experimental evidence of nutrient energy-dependent biologically-based cause and effect has supported the constraint-breaking mutation claim. All experimental evidence of nutient energy-dependent biologically-based cause and effect has supported my claims about the role that RNA-mediated amino acid substitutions play in the nutrient-dependent pheromone-controlled organization and activation of supercoiled DNA in all living genera.
For example, on June 13, 2014, this article was published. Strong male bias drives germline mutation in chimpanzees
Germline mutation determines rates of molecular evolution, genetic diversity, and fitness load.
My comment: This forced a change in the representations made by neo-Darwinian theorists. The change was reported as: Human & Chimp Genes May Have Diverged Twice As Long Ago As We Thought.
Less than one year after comparisons of our divergent conclusions could have been made, the problem with Nei’s misrepresentations in Mutation-driven evolution became clear. Supposedly, mutations must accumulate before they somehow cause a species-wide change, but examples of nutrient-dependent amino acid substitutions that alter cell type differentiation show how quickly fixation occurs via the physiology of reproduction. Thus, the time frame for species-wide fixation of mutations, which no experimental evidence suggests ever occurs, must be extended.
If animal models are used by theorists to teach people about the pseudoscientific nonsense that population geneticists invented to explain ecological adaptations, they must keep trying to link mutations from ecological variation to to energy-dependent ecological adaptations. However, assertions that the mutation-driven evolution of biodiversity is an established fact can be compared to what is known by serious scientists.
For comparison, see:
My comment: For an example of what happened in less than two years after comparisons could have been made between the conclusions from 1) Nutrient-dependent/pheromone-controlled adaptive evolution: a model and 2) Mutation-Driven Evolution,
- When proteins and sugars are mixed together and heated, new chemical compounds are formed
- …our findings represent a real advance in the area of milk proteins and indicate that f-cMRP and cMRP could be recommended for use as potential antioxidants and cardioprotective ingredients for various functional, pharmaceutical, and dairy applications.
My comment: Nutrient energy-dependent thermodynamic cycles of protein biosynthesis and degradation are perturbed by virus-driven energy theft, which is why it is important to know that the bull sperm microRNAome and brain development in human infant is linked by the energy-dependent changes in microRNAs in breast milk, which are linked to the human microRNAome via everything currently known about metabolic networks and genetic networks in all living genera.
For an example of what happened in less than 3 years after comparisons could have been made between the conclusions from 1) Nutrient-dependent/pheromone-controlled adaptive evolution: a model and 2) Mutation-Driven Evolution,
See: Epigenetics and Genetics of Viral Latency (May 11, 2016)
…viral latency is responsible for life-long pathogenesis and mortality risk…
My comment: Transgenerational epigenetic inheritance of virus-driven DNA damage is exemplified in the craniofacial deformities linked from the Zika virus to the development of the human brain.
See also: Kinds of top-down causation with my emphasis (June 1, 2016)
The selection of native nucleic acid folding (an irreducible higher level variable) is an epigenetic effect,with broad implications for the evolution of plants and their viruses. The folding structure (a higher level variable) corresponds to an equivalence class of lower level sequences, and is the biologically relevant variable determining the selection that occurs. How do we demonstrate this top-down causation? This has been shown in detail experimentally by Shepherd et al. .
My comment: George Ellis admits that he knows about the experimental evidence of top-down causation that Shepherd et al. (2006) linked from energy-dependent biophysically constrained protein folding chemistry via nucleic acid folding conservation. The authors claimed that nucleic acid folding conservation:
…is the selective principle behind a high-frequency single-nucleotide reversion observed in a three-nucleotide mutated motif of the Maize streak virus replication associated protein (Rep) gene. In silico and in vitro studies showed that the three-nucleotide mutation adversely affected Rep nucleic acid folding, and that the single-nucleotide reversion [C(601)A] restored wild-type-like folding.
See also: In the present study, the effects of a two amino acid substitution (LLCNE to LLCLK) in the MSV RepA pRBR-interaction motif on both virus replication in maize culture cells and infectivity in maize were determined.
My comment: They linked a single energy-dependent nucleotide reversion to repair of DNA damage via the effects of a two amino acid substitution. Questions about what caused the DNA damage have only recently begun to be asked. Neo-Darwinian theorists simply assumed that mutations caused the DNA damage and that beneficial mutations were naturally selected. In other words, they assumed that all energy-dependent biodiversity could be explained in the context of the emergence of the first cell and mutation-driven evolution of all other cell types.
See also: The Broader View – with my emphasis (June 1, 2016)
The conclusion arising from the arguments given in this book is that there are other forms of causation than those encompassed by physics and physical chemistry alone, or even in genetics and neuroscience.
…a discrete biological function can only rarely be attributed to an individual molecule, in the sense that the main purpose of haemoglobin is to transport gas molecules in the bloodstream. In contrast, most biological functions arise from interactions among many components. For example, in the signal transduction system in yeast that converts the detection of a pheromone into the act of mating, there is no single protein responsible for amplifying the input signal.
My comment: Ellis quotes from: Hartwell et al. (1999) From molecular to modular cell biology.
Finally, we emphasize the importance of integrating experimental approaches with modelling and conceptual frameworks. The best test of our understanding of cells will be to make quantitative predictions about their behaviour and test them. This will require detailed simulations of the biochemical processes taking place within the modules. But making predictions is not synonymous with understanding. We need to develop simplifying, higher-level models and find general principles that will allow us to grasp and manipulate the functions of biological modules. The next generation of students should learn how to look for amplifiers and logic circuits, as well as to describe and look for molecules and genes (Box 3). Connecting different levels of analysis — from molecules, through modules, to organisms — is essential for an understanding of biology that will satisfy human curiosity.
My comment: There is no evidence presented in the book that Ellis is beginning to understand what is known to many others about energy-dependent biologically-based cause and effect. How could he not?
He already acknowledged the two most important claims I made in the context of Understanding and accounting for relational context is critical for social neuroscience
See the comments section:
- This is absolutely correct and forms part of the larger concept that top-down causation is a key factor not just in the way the brain works but in broader contexts in biology and even physics.
- Great links, thanks. I’m intrigued by your work on pheromones. It is just possible it might relate to the issue of primordial emotional systems…
I responded: Start with yeasts: Signaling Crosstalk: Integrating Nutrient Availability and Sex The nutrient-dependent production of the alpha mating pheromone exemplifies cell type differentiation at the advent of sexual reproduction, and when concentrated it elicits a luteinizing hormone (LH) response from the cultured pituitary cells of a mammal, the rat.
Tomorrow marks the third anniversary during which my review has been ignored by people like George Ellis, who still seem to be trying to defend ridiculous theories that have never integrated experimental evidence of biologically-based cause and effect.
See also: Destiny Isn’t Completely Written in Your Genes (June 10, 2016)
“Your genes are profoundly important in determining your future, but the workings of the cell are complex and those sequences are not all that’s in play.”
…the long gene list we discovered should serve as an important launching point for future studies into the still mysterious molecular mechanisms underlying learning and memory.
My comment: They link the conserved molecular mechanisms of epigenetically-effected RNA-mediated learning and memory to this representation of biologically-based cause and effect.
The honeybee already serves as a model organism for studying human immunity, disease resistance, allergic reaction, circadian rhythms, antibiotic resistance, the development of the brain and behavior, mental health, longevity, diseases of the X chromosome, learning and memory, as well as conditioned responses to sensory stimuli (Kohl, 2012). — Nutrient-dependent/pheromone-controlled adaptive evolution: a model (2o13).
…certain genes involved in creating long-term memories in the brain are the same ones that the eye uses for sensing light.
Although studies in other organisms, including humans, have detected sensory genes in areas of the brain unrelated to the sensory organ itself, this may be the first study to link these genes to memory formation.
My comment: Anna Di Cosmo, John Hewitt, Luca Turin, and Tim Bredy, will be able to link this from quantized energy-dependent changes in hydrogen-atom transfer in DNA base pairs in solution to ecological, social, neurogenic, and sociocognitive niche construction in species from microbes to humans via the conserved molecular mechanisms of RNA-mediated cell type differentiation they have learned about.
Unfortunately, many other researchers will not recognize that the quantized energy-dependent de novo creation of G protein-coupled receptors links chemotaxis to phototaxis in that order. That’s why others do not seem to know that the virus-driven theft of quantized energy is linked to all pathology. They’ve been taught that humans are primarily visual creatures in the context of ridiculous theories, like the one that links “Quantum Darwinism” from natural selection to the mutation-driven evolution of biodiversity.
NASA, Jesus & Templeton? (June 3, 2016)
Religion has nothing to do with science and the NASA Astrobiology Program has squandered precious public funds — 5% of its annual budget — for an investigation into how the world’s religions might respond to the discovery of life on other planets. It has handed over $1.108M to a religious think tank, a nonprofit corporation with wealth management professionals on its board that already has in excess of $23M in assets.
My comment: Young earth creationists linked virus-driven energy theft to all pathology in “Viral Genome Junk Is Bunk”
I repeat: Paul M. Lieberman did that in “Epigenetics and Genetics of Viral Latency”
See also: What is life when it is not protected from virus driven entropy
Templeton funds those who keep the focus on “Quantum Darwinism” instead of Schrodinger’s claims about the anti-entropic quantized energy of sunlight in “What is Life?” (1944). For example, the effects of virucidal UV light have been linked from RNA-mediated DNA repair to biophysically constrained energy-dependent cell type differentiation in all living genera.
When energy-dependent microRNA flanking sequences are linked to learning and memory, questions about the connection between morphological and behavioral biodiversity will be answered in the context of Darwin’s nutrient energy-dependent “conditions of life” and the physiology of reproduction, which links supercoiled DNA to the protection of all organized genomes from virus-driven energy theft and genomic entropy. I don’t think those answers will lie outside the context of what most creationists have been taught to believe.