A reversible TCA cycle in a thermophile

Make no mistake, pseudoscientists have stolen the soul of science for more than 20 years, with their ridiculous claims about mutations and evolution.
For comparison, see:

“…considering that we have just 3 such round Nos ‘100’ ‘1000’ ‘10000’, its just three out of all realistic possibilities, no? Admit its looks cool just bec. we calc in Dec system. History books claims was invented by ancient societies; but I think its evolution: We have 10 fingers!”

My reply (SARCASM ALERT):

Thanks. The correlations are intriguing. Templeton funding might help you prove that the numbers game of evolution is true in the context of Cosmopsychism. With enough correlations, facts that link physics and chemistry to viral latency can be dismissed.

Thanks to the Ralser lab for bringing this to my attention with a claim about:
A reductive TCA cycle in a thermophile, which uses the same citrate synthase [enzyme] both for the oxidative and the reductive directionality.

“Every day it looks more likely that primoridial and modern metabolism look similar”

A link was provided to: A primordial and reversible TCA cycle in a facultatively chemolithoautotrophic thermophile

…raises the possibility of a facultatively chemolithomixotrophic origin of life.

Has anyone else considered that possibility?
I tried to look at it from the perspective of chemoorganoheterotrophic metabolism and electron-eating microbes that enzymatically (not automagically) create uranium isotopes, but I got side-tracked by the claims about mutations and evolution. I could not link those claims from the physiology of reproduction in microbes to claims that link the metabolism of food energy to pheromones that biophysically constrain viral latency in species from microbes to humans.

Now, the physiology of pheromone-controlled reproduction in electron-eating microbes that create uranium isotopes suggests the same thing that the Ralser lab suggested: SARCASM ALERT: “It’s turtles all the way down” (the infinite regress problem in cosmology).Unless, like the folks at the Ralser Lab,  you are a serious scientist.

The problem for pseudoscientists, theorists, and many so-called science journalists may be familiar to those at the Ralser lab. McEwen et al., (1964) reported “The synthesis of RNA in isolated thymus nuclei is ATP dependent.” All serious scientists know “ATP controls the crowd.”

These findings suggest an additional way for cells to use ATP to maintain proteostasis in the crowded cytoplasm and also fine-tune the material properties of nonmembrane-bound organelles and the cell interior in general.

Obviously, there are now several groups of serious scientists that can make fun of all the pseudoscientists and so-called science journalists who have failed to link physics and chemistry to biophysically constrained viral latency via energy-dependent changes in base pairs in species from thermophiles to those that create uranium isotopes. But Kudos to the first group, or one of the first, to do that:

12/10/14 All about that base and Structural diversity of supercoiled DNA 10/12/15

Sarcasm Alert: I hope that claims about the emergence of energy and mutation-driven evolution did not confuse others as much as they confused so-called science journalists such as John Hewitt, Philip C. Ball, Carl Zimmer, and many others.
When you see the facts reported by an intelligent science journalist, please tell others about the claims that link the creation of energy from the game “Subatomic” to biophysically constrained viral latency in “Cytosis.” Comparisons will be made. It will become clearer that pseudoscientists, theorists and many others have lost their games.
See for example: Attacked from All Sides: RNA Decay in Antiviral Defense

…RNA decay machinery plays important roles in antiviral defense. This can involve either direct effects on vRNA stability or indirect regulation of the intracellular milieu. Furthermore, an emerging theme suggests that many RNA binding proteins can be repurposed from their endogenous roles in the nucleus to antiviral roles in the cytoplasm. Future studies are necessary to further elucidate how these RNA binding…

…proteins recognize foreign RNAs and how they interface with the RNA decay machinery to restrict vRNA replication.”

Alternatively, everyone can simply accept the fact that food energy typically restricts the virus-driven degradation of messenger RNA, and tell all the pseudoscientists and so-called science journalists where to put their pseudoscientific nonsense (e.g., where the sun don’t shine).
For example: Is the Universe a conscious mind?

Cosmopsychism might seem crazy, but it provides a robust explanatory model for how the Universe became fine-tuned for life

For comparison: A Big Bang in spliceosome structural biology and Alternative splicing and the evolution of phenotypic novelty
But remember to link the claims about the evolution of phenotypic novelty to the missing claims about behavior, and see the claims made by Bruce McEwen and Martin Picard in:
Psychological Stress and Mitochondria: A Conceptual Framework (Part 1)

Mitochondria, a subcellular organelle with its own genome, produce the energy required for life and generate signals that enable stress adaptation. An emerging concept proposes that mitochondria sense, integrate, and transduce psychosocial and behavioral factors into cellular and molecular modifications. Mitochondrial signaling might in turn contribute to the biological embedding of psychological states.

Reported as: Cellular ‘powerhouses’ may explain health effects of stress
in the same context as Psychological Stress and Mitochondria: A Systematic Review (Part 2)

Evidence from metabolomic, proteomic, and transcriptomic studies also suggest additional layers of regulation by which stressful experiences may alter mitochondrial components among rodents. Although these metabolites, protein composition, and gene expression outcomes do not reflect the functionality of mitochondria, when assessed in parallel with functional outcomes, they will help explain and refine our understanding of the mechanisms by which stress influences mitochondrial function and health. In addition, whereas functional changes should be regarded as primary indicators of MAL (21), stress-induced molecular changes within mitochondria may also reflect compensatory mechanisms or recalibrations that contribute to long-term changes in mitochondrial function and to the accumulation of MAL. [mitochondrial allostatic load (MAL)]