Caption: Contemporary analyses of cell metabolism have called out three metabolites: ATP, NADH, and acetyl-CoA, as sentinel molecules whose accumulation represent much of the purpose of the catabolic arms of metabolism and then drive many anabolic pathways. Such analyses largely leave out how and why ATP, NADH, and acetyl-CoA (Figure 1) at the molecular level play such central roles. Yet, without those insights into why cells accumulate them and how the enabling properties of these key metabolites power much of cell metabolism, the underlying molecular logic remains mysterious. Four other metabolites, S-adenosylmethionine, carbamoyl phosphate, UDP-glucose, and Δ2-isopentenyl-PP play similar roles in using group transfer chemistry to drive otherwise unfavorable biosynthetic equilibria. This review provides the underlying chemical logic to remind how these seven key molecules function as mobile packets of cellular currencies for phosphoryl transfers (ATP), acyl transfers (acetyl-CoA, carbamoyl-P), methyl transfers (SAM), prenyl transfers (IPP), glucosyl transfers (UDP-glucose), and electron and ADP-ribosyl transfers (NAD(P)H/NAD(P)+) to drive metabolic transformations in and across most primary pathways. The eighth key metabolite is molecular oxygen (O2), thermodynamically activated for reduction by one electron path, leaving it kinetically stable to the vast majority of organic cellular metabolites

Odor activation of ATP (2)

Metabolic Regulation of Cytoplasmic DNA Synthesis (1974)

The curve that results when the rate of DNA synthesis is plotted as a function of ATP concentration is sigmoidal, suggesting that more than one site on the enzyme interacts with ATP and that these sites are acting cooperatively.

Odor activation of ATP is the obvious link to RNA-mediated feedback loops that control the food energy-dependent pheromone-controlled physiology of reproduction via the rate of DNA repair in species from microbes to humans.
See: “ATP activation
See for comparison: Feedback loops link odor and pheromone signaling with reproduction (2005)
See also: “ATP activation” microRNA
See also: Mapping malaria by combining parasite genomic and epidemiologic data

Here, we discuss the spatial epidemiology of malaria in the context of transmission-reduction interventions, and the challenges and promising directions for the development of integrated mapping, modeling, and genomic approaches that leverage disparate data sets to measure both connectivity and transmission.

The sun’s anti-entropic virucidal energy has been linked to protective food energy-dependent hemoglobin variants via 1700+ examples. The variants link interethnic similarities and differences to all extant human populations.
HbVar: A Database of Human Hemoglobin Variants and Thalassemias
SNPs or indels [insertions/deletions] link amino acid substitutions to hemoglobin variants. Molecular defects [mutations] in regulatory or coding regions of the human genes can minimally or drastically reduce their expression, leading to α-, β- or δ-thalassemia, respectively.
What can be said about so-called scientists and so-called science journalists who do not know the difference between how a food energy-dependent amino acid substitution is linked to ecological adaptations and how a mutation is linked to diseases?
Who was the first to say it?

Who will be the next to disagree:
Jay R. Feierman:

Variation is not nutrient availability and the something that is doing the selecting is not the individual organism. A feature of an educated person is to realize what they do not know. Sadly, you don’t know that you have an incorrect understanding [of] Darwinian biological evolution.

Darwin repeatedly asserted that “conditions of life” must be placed before natural selection. Without the sun’s anti-entropic energy, no species on Earth can adapt to ecological variation.

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