The screenshot (above) links 7+ years of Jon Lieff’s pseudoscientific nonsense about millions of years of evolution to accurate representations of energy-dependent biophysically constrained microRNA-mediated healthy longevity.
A screening error? See for comparison my response to the pseudoscientific nonsense touted in many other bioRxiv preprints. Finally, someone got it right, on 11/30/19!
See for comparison: Olfaction Warps Visual Time Perception 5/1/18
The energy-dependent Creation of enzymes was linked from Creation of the sense of smell in bacteria to to our visual perception of energy and mass across the space-time continuum.
It makes no sense for theorists to claim they will never stop trying to link the emergence of energy from the void to the evolution of “our Multiverse.” But the clear statement of ill-will (above), and the retraction can be compared to what is known to all serious scientists via the following publications.
Simply put, every aspect of Creation starts from the light-activated assembly of the microRNA-RNA-peptide nanocomplex, which biophysically constrains viral latency in the context of autophagy.
See: MicroRNAs biophysically constrain Virus-driven pathology (4) 11/30/19 and:
The degraded endoplasmic reticulum fragments can be reassembled into a new endoplasmic reticulum to restore the normal state of it. Hence, it seems that the autophagy has become the last mean to restore the homeostasis of endoplasmic reticulum.
The reassembly of viruses and viral fragments in vaccines prevents the restoration of homeostasis by altering the energy-dependent reassembly.
To adapt to these stimuli, maintain physiological stability, and ensure survival, cells in the body initiate a series of interactive and regulatory response pathways. For example, increased reactive oxygen species in the body can induce autophagy through a variety of signalling pathways.
If so, how does one species evolve into another?
Cells degrade harmful intracellular components with the aid of autophagy to maintain a healthy state. In recent decades, the study of non-coding RNA in the regulation of autophagy has been a hot area. Mounting evidence indicates that many ncRNAs are involved in the dynamic process of autophagy, and further studies were undertaken to dissect the detailed cellular and molecular mechanisms underlying this process. In this chapter, we mainly summarized the regulation of different non-coding RNAs in autophagy as well as the detailed mechanisms.
I repeat the question: “…how does one species evolve into another?”
PTM includes an attachment of addition of functional groups, such as methylation, acetylation, glycosylation and phosphorylation; a covalent coupling of small peptides or proteins, such as ubiquitination and SUMOylation; or chemical changes in amino acids, such as citrullination (conversion of arginine to citrulline).
The number of chemical changes that link phosphorylation to fixation of amino acid substitutions turned out to be incalculable. See:
Strong anion exchange-mediated phosphoproteomics reveals extensive human non-canonical phosphorylation 8/21/19, which was reported on 11/4/19 as: Cell signalling breakthrough opens up new avenues for research
…the phenomenon of protein modification (phosphorylation) in cell signalling is far more diverse and complex than previously thought.
…various environmental signaling pathways are somehow integrated with autophagy signaling, such as the lack of nutrients (amino acids or glucose or others), changes in pH or osmotic pressure. Autophagy has been seen as an adaptive response to stress.
Adaptations are food energy-dependent and pheromone-controlled in species from microbes to humans, and they occur too quickly to be placed back into the context of ridiculous theories. See for instance: Bacteria evolve over a weekend 2/26/15 (video)
All the mechanisms are energy-dependent and they link the light-activated assembly of the microRNA-RNA-peptide nanocomplex to biophysically constrained viral latency and healthy longevity via the physiology of reproduction.
Autophagy is an evolutionarily conserved lysosome-dependent intracellular degradation process that is essential for the maintenance of cellular homeostasis and adaptation to cellular stresses in eukaryotic cells. The most well-characterized type of autophagy, the macroautophagy, involves the progressive sequestration of cytoplasmic components into dedicated double-membraned vesicles called autophagosomes, which ultimately fuse with lysosomes to initiate the autophagic degradation of the sequestered cargo. In the past decade, our understanding of the molecular mechanism of macroautophagy has significantly evolved, with particular contributions from the biochemical and structural characterizations of autophagy-related proteins. In this chapter, we focus on some autophagy regulatory proteins involved in the macroautophagy pathway, summarize their currently known structures, and discuss their relevant molecular mechanisms from a perspective of structural biology.
Unless the pathway and the proteins simultaneously and automagically evolved, food energy-dependent pheromone-controlled autophagy is not an evolutionarily conserved process for adaptation to stress.
For comparison, see: Codon identity regulates mRNA stability and translation efficiency during the maternal-to-zygotic transition 7/9/16
Everything known to serious scientists suggests this code integrates multiple sensory inputs that link the ATP-dependent creation of RNA from tRNA modification to the availability and accuracy of amino acid identity, which links peptide bond formation to the creation of all proteins.
That is what natural selection for energy-dependent codon optimality does in species from microbes to humans via autophagy, not via the evolution of proteins.