Biophotonics, glycobiology, quantized biodiversity

By: James V. Kohl | Published on: July 31, 2016

Historical perspective: From Fertilization to Adult Sexual Behavior

Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to sexual differentiation in at least two species, Drosophila melanogaster and Caenorhabditis elegans (Adler and Hajduk, 1994; de Bono, Zarkower, and Hodgkin, 1995; Ge, Zuo, and Manley, 1991; Green, 1991; Parkhurst and Meneely, 1994; Wilkins, 1995; Wolfner, 1988). That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes.

My comment: I do not know any serious scientist who claims that protein folding chemistry is not energy-dependent and RNA-mediated or that it does not involve alternative splicings of pre-mRNA.
See for comparison:

Protein folding video misrepresentation (4 minutes)

My comment: The most recent misrepresentation of protein folding chemistry links two mutations from amino acids to co-evolution.

There is no magic in protein folding; it is energy-dependent. All misrepresentations fail to link what is known about biophysically constrained energy-dependent protein folding chemistry to cell type differentiation via RNA-mediated amino acid substitutions. Instead, the misrepresentations are consistently used to support ridiculous theories about evolution outside the context of virus-driven energy theft and genomic entropy.

The ignorant masses of biologically uninformed pseudoscientists and laypersons are led to believe in the pseudoscientific nonsense of neo-Darwinian theory. And yet, few people respond to my  accurate representations of biologically-based cause and effect in my FB posts or blog posts about articles like this one:

Epigenetics and Genetics of Viral Latency


“…viral latency is responsible for life-long pathogenesis and mortality risk…”

My comment: I would like to be polite about the consequences of knowing that. Does everyone accept the fact that their ignorance is killing them?
If you don’t want to suffer and die from a preventable early death, see:

Special Report on Cell Biology: Sweetening the pot

My comment: This comprehensive report links nutritional epigenetics from energy-dependent metabolic networks to genetic networks in all living genera. It stops short of placing what’s known about energy-dependent RNA-mediated cell type differentiation into the context of links from the innate immune system to supercoiled DNA.
The supercoiled DNA protects all organized genomes from virus-driven entropy. Schrodinger’s claims from 1944 and the comment by Roger Penrose in the forward to the reprint of “What is Life?” can now be placed into the contest of information as nutrient-dependent energy that regulates the transgenerational epigenetic inheritance of mRNA stability and translation efficiency.
Finally, others have learned how to link energy-dependent changes in the microRNA/messenger RNA balance from RNA methylation to learning and memory via the function of the innate immune system. Proper function links the immune system from the physiology of reproduction to fixation of RNA-mediated amino acid substitutions in the supercoiled DNA that protects all organized genomes from virus-driven energy theft and genomic entropy.
See for examples: (2010) Mystery RNA spawns gene-activating peptides

This finding has echoes of the paradigm-changing discovery of the small non-coding RNAs called microRNAs, which have direct gene-regulatory functions.

See also: (2014) Redundancy of the genetic code enables translational pausing
Abstract excerpt:

The codon redundancy (“degeneracy”) found in protein-coding regions of mRNA also prescribes Translational Pausing (TP). When coupled with the appropriate interpreters, multiple meanings and functions are programmed into the same sequence of configurable switch-settings.

See also: (2014) Identification of small ORFs in vertebrates using ribosome footprinting and evolutionary conservation


Central roles of small peptides have been known for decades based on the importance of neuropeptides, peptide hormones (such as secretin or insulin) and secreted signaling molecules (such as FGF1). However, the majority of these small peptides are encoded as large pre‐proteins that undergo post‐translational cleavage and modification. By contrast, similar functional small peptides such as ELABELA/toddler (Chng et al, 2013; Pauli et al, 2014) (also identified in our set of smORFs; Supplementary Fig S3) are directly translated from small ORFs. Indeed, Pauli et al (2014) recently reported the independent identification of more than 300 previously unannotated zebrafish proteins. Small proteins are also found in viral genomes, where transmembrane proteins (often shorter than 50 aa) have been shown to play vital roles in virus replication and virulence (Dimaio, 2014).

See also (2016) Chromatin controls behavior

reported as: Ability to turn off genes in brain crucial for learning, memory

One process that controls chromatin structure and transcription is chromatin remodeling by energy-dependent protein complexes (4). Such complexes that depend on adenosine 5′-triphosphate (ATP) can control gene expression by moving, ejecting, or restructuring nucleosomes, the scaffolds around which DNA wraps. Each nucleosome contains a core particle of eight histone protein subunits (5). Remodeling events include posttranslational modifications, swapping individual histone subunit isoforms into and out of the core particle, and facilitating the unbinding of DNA from the core particle.

My comment: Word choice and omissions are a form of wordplay for those who know better than to refute neo-Darwinian nonsense by substituting ‘histone subunit isoforms’ for claims about RNA-mediated amino acid substitutions.
Google:histone subunit isoform” in an attempt to find what you were just told linked energy-dependent changes in chromatin from learning and memory to behavior. For an even clearer indication of the games academics play with works, find the newly invented term.
Here, let me help:  An oncohistone deranges inhibitory chromatin

Missense mutations (that change one amino acid for another) in histone H3 can produce a so-called oncohistone…

My comment: Mutations do not change one amino acid for another in organized genomes, which is why the result of a missense mutations is called an oncohistone.  They use a form of evolutionary double-speak to link mutations and RNA-mediated amino acid substitutions to a negative outcome because virus-driven energy theft causes the mutations, and nutrient energy-dependent RNA-mediated cell type differentiation prevents the mutations. If energy-dependent RNA-mediated DNA repair did not occur, the virus-driven energy theft would bring all life on Earth to a fast and very unpleasant end. All organisms would suffer to the degree that any species can suffer, and all species would become extinct.
See also: What is life when it is not protected from virus driven entropy

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