Any anonymous participant in the discussion of: DNA may have had humble beginnings as nutrient carrier (Sep 01, 2014 by Adam Hadhazy) asks:
“when are you going to keep quiet?”
In a series of responses, I have explained the problem I have with honoring his request.
The following excerpts from Wikipedia and other sources are loosely strung together because there is no point to providing more extensive details of biologically-based cause and effect until others accept the fact that mutations and natural selection cannot lead to the evolution of biodiversity. Even without accepting the fact that nutrient-dependent amino acid substitutions differentiate the cell types of all individuals in all species, it should be clear that mutations do not. Until that fact becomes clear, nothing known about physics, chemistry, and molecular biology can be used to refute ridiculous theories. Here are examples of what cannot be used.
1) In mammals, phosphatidylserine is produced by base-exchange reactions with phosphatidylcholine and phosphatidylethanolamine. The products of this reaction are novel dinucleotides. Nicotinamide adenine dinucleotide (NAD) is a coenzyme found in all living cells. (The compound is a dinucleotide, since it consists of two nucleotides joined through their phosphate groups.)
The flipping of one base pair appears to result in Fragile X Syndrome, which is the most common form of mental retardation. It may represent what happens when an atomic-level change in nutrient-dependent energy perturbs protein folding.
For comparison, the nutrient-dependent flipping of a base pair associated with vitamin C uptake in mammals links frugivory in bats via morphological and behavioral phenotypes to their adaptive radiations. Their phenotypes link nutrient-dependent pheromone-controlled reproduction in all vertebrates and invertebrates to morphological and behavioral changes during the development of human preferences for food odors and pheromones.
2) Rather than be quieted by the pseudoscientific nonsense of evolutionary theorists who want others to believe that mutations and natural selection lead to the evolution of biodiversity, ecologists and other serious scientists continue to link biologically-based cause and effect from atoms to ecosystems via the conserved molecular mechanisms of amino acid substitutions that I detailed in my model.
Serious scientists know that models will lead to atomic level (nutrient-dependent) cures for diseases and disorders that evolutionary theorists claim are due to the same molecular mechanisms they think must link mutations to increasing organismal complexity manifested in morphological and behavioral phenotypes of species from microbes to man.
The difference between a serious scientist and a theorist (or any other idiot) is recognized by differences in their beliefs about biologically-based cause and effect. Theorists have no understanding of links between atoms and ecosystems; serious scientists attempt to understand the experimental evidence.
3) In metabolism, nicotinamide adenine dinucleotide is involved in redox reactions, carrying electrons from one reaction to another.
Most organisms synthesize NAD+ from simple components. The specific set of reactions differs among organisms, but a common feature is the generation of quinolinic acid (QA) from an amino acid—either tryptophan (Trp) in animals and some bacteria, or aspartic acid in some bacteria and plants.
Besides assembling NAD+ de novo from simple amino acid precursors, cells also salvage preformed compounds containing nicotinamide. Despite the presence of the de novo pathway, the salvage reactions are essential in humans; a lack of niacin in the diet causes the vitamin deficiency disease pellagra. This high requirement for NAD+ results from the constant consumption of the coenzyme in reactions such as posttranslational modifications, since the cycling of NAD+ between oxidized and reduced forms in redox reactions does not change the overall levels…
4) Rather than continue to examine facts that link the thermodynamic cycles of protein biosynthesis and degradation from atoms to ecosystems via organism-level thermoregulation, others may want to consider the alternative.
In “Mutation-Driven Evolution” for example, the claim is made that “…genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world.”
That claim is not supported by any experimental evidence of biologically-based cause and effect, but many evolutionary theorists are convinced that the differences in morphology and behavior they can see are due to mutations that perturb protein folding at the level detailed in the Laws of Physics, which lead to everything known about chemistry and Kohl’s Laws of Biology, which are linked to the de novo Creation of olfactory receptor genes via the de novo Creation of RNA and DNA.
Addendum: Anyone willing to accept the fact that RNA and DNA somehow ‘evolved’ or that what’s known about the biophysical constraints that link ecological variation to ecological adaptations via conserved molecular mechanisms in species from microbes to man is not likely to lead to cures for diseases and disorders associated with mutations should participate in discussions on blog sites run by atheistic biology teachers like PZ Myers. For example see: One crank dies, another rises to take his place. Anyone willing to accept the fact that RNA and DNA were Created should examine the content of articles that represent what is known about the Laws of Physics; what is known about chemistry; and what is known about molecular biology. See for example: Darwin vs. Genetics: Surprises and Snags in the Science of Common Ancestry
In the context of biophysically-contrained ecological adaptations it may interest others to learn what is obviously missing from what’s being billed as the Theory of Everything. A theory of everything should have some explanatory power in the context of biologically-based cause and effect that does not link perturbed protein and nutrient-dependent ecological variation to pheromone-controlled ecological adaptations via the same molecular mechanisms. What if Hawkings’ disabled body could be linked from epigenetically-effected RNA and DNA to his highly functional mind? Would others be more interested in biological facts about the de novo Creation of proteins that can be compared to his theory of everything?
What if a nutrient-dependent flip in a single base pair led to amino acid substitutions that differentiate all the cell types of all individuals of all species via conserved molecular mechanisms? Could the link from Fragile X Syndrome and mental retardation be the same as the link to hemoglobin S and nutrient-dependent brain development in someone like you, or like Hawkings? If so, the link is likely to be nutrient-dependent amino acid substitutions that differentiate all cell types in all tissues of all organs in all organ systems of invertebrates and vertebrates via conserved molecular mechanisms of pheromone-controlled reproduction.
We can see the origins of that perspective on autophagy, which was the basis for my works in these two published works.
My comment: Both were co-authored by Bruce McEwen. He told me in 1991 that I would need to start with energy-dependent gene activation before my model of cell type differentiation could be completely validated. I did that in the following year with the help of Robert L. Moss and his co-authors in a series of published works that linked pheromones to gene activation in GnRH neurosecretory neurons of the mammalian hypothalamus.