Kohl and Francoeur at 25 (5)

By: James V. Kohl | Published on: April 2, 2019

A Quick HYL1-Dependent Reactivation of MicroRNA Production Is Required for a Proper Developmental Response after Extended Periods of Light Deprivation

…plants alter microRNA (miRNA) biogenesis in response to light transition.

Light-tracking Brugmansia need only sunlight (subatomic particles) and water to grow in buckets. The subatomic particles link cytosis to biophysically constrained viral latency

See also: YY1 Is a Structural Regulator of Enhancer-Promoter Loops

…the ubiquitously expressed transcription factor Yin Yang 1 (YY1) contributes to enhancer-promoter structural interactions in a manner analogous to DNA interactions…

Intelligent people know that the YY1 transcription factor (i.e., the structural regulator) cannot regulate the creation of the energy-dependent microRNA-mediated functional structure of supercoiled DNA. The intelligent people started  Rethinking transcription factors and gene expression.
The intelligent people noted that:

“Hundreds of scientific papers have linked YY1 dysfunction to diseases such as viral infections, cancer, and arthritis, and yet the studies produced seemingly contradictory observations of YY1’s function.”

It should be clear that Yin Yang dysfunction is linked to autophagy dysfunction via the virus-driven degradation of messenger RNA. That is how energy-dependent YY1 function is linked to healthy longevity and how the virus-driven degradation of messenger RNA is linked from mutations to virus-driven disease.
See also:  The small peptide world in long noncoding RNAs

One study identified a 46-aa-long evolutionarily conserved peptide from an lncRNA. This peptide, named myoregulin (MLN), interacts with the sarcoendoplasmic reticulum calcium transport ATPase (SERCA) calcium-ATPase and inhibits calcium reuptake into the sarcoplasmic reticulum [57].

These so called evolutionarily conserved interactions are energy-dependent. But the energy-dependent biophysical constraints on the creation of the 46-amino acid-long peptide are placed back into the ridiculous context of evolutionary conservation.
In their discussion of these findings, the authors claim that:

LncRNAs, or the peptides coded by them, are expected to be the missing pieces of many molecular mechanisms.

Only if the light-activated assembly of the microRNA-RNA-peptide nanocomplex links the coded creation of peptides to amino acids can the peptides be the missing links.
For comparison, see: A universal trend of amino acid gain and loss in protein evolution

Amino acid composition of proteins varies substantially between taxa and, thus, can evolve.

Where do pseudoscientists get the idea that variations in the peptides of the amino acid compositions automagically evolve?
See how pseudoscientific nonsense begets more pseudoscientific nonsense in: Codon Optimality Confers GC-Rich-Induced Stability to mRNAs in Humans (3/24/19)

Assuming that evolution drives the selection of codons, synonymous codon usage in different organisms must be fine-tuned over time to achieve precise expression levels of mRNA and eventually proteins in essential physiological process.

What kind of biologically uninformed science idiot assumes that evolution drives the selection of codons? Serious scientists know that natural selection for energy-dependent codon optimality links pheromone-constrained viral latency to transgenerational epigenetic inheritance in species from microbes to humans.
See: Codon identity regulates mRNA stability and translation efficiency during the maternal‐to‐zygotic transition (10/4/16)

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