The stability of organized genomes (4)

(click to enlarge)

Note: Replication stress can be linked from nutrient stress or from social stress to thermodynamic cycles of protein biosynthesis and degradation. Stress induced pathologies arise in the context of virus perturbed protein folding, Healthy longevity arises in the context of nutrient-dependent RNA-mediated gene duplication and fixation of RNA-mediated amino acid substitutions in organized genomes via the physiology of reproduction. Others have now linked stress to cancer but they have not linked RNA-mediated amino acids substitutions and ecological adaptations to healthy longevity via DNA repair.

Replication stress in early S phase generates apparent micronuclei and chromosome rearrangement in fission yeast OPEN ACCESS

Excerpt:

These observations have led to the suggestion that aberrant micronucleus segregations are associated with the catastrophic chromosome rearrangements

Reported as: Mutant cells that can’t copy DNA somehow keep dividing when they shouldn’t—with disastrous consequences

Excerpt: 

…a mutation in the yeast’s MCM helicase triggered responses similar to those in mammals

where mutations in this gene are associated with cancer and the formation of micronuclei.

My comments:
1) At the advent of sexual reproduction in yeast, their morphological and behavioral phenotypes are nutrient-dependent and pheromone-controlled via the physiology of their reproduction. So far as I know that is how all cell type differentiation is controlled in species from microbes to man.Nutrient-dependent RNA-mediated gene duplication and RNA-mediated amino acid substitutions appear to link cell type differentiation from the epigenetic landscape to the physical landscape of DNA in all living genera.
Isn’t it likely that viruses have caused the damage to the problematic DNA and that the damage is not being repaired as it typically would be via RNA-mediated events linked from ecological variation to ecological speciation via the conserved molecular mechanisms of biophysically constrained protein folding chemistry that is perturbed by viruses?
2) Excerpt: “The devil’s in the division. In real time, we’re able to see that these mutant cells ignore the damage caused during DNA replication, which results in the creation of unusual structures… ”
My comment: I hesitate to invite the trolls by mentioning that this appears to be consistent with a young earth creationist perspective on virus-perturbed cell type differentiation.
Excerpt: “In other words, mammalian viruses may not have existed at all before the Curse, but after mankind’s sin may have been allowed to develop from DNA sequence already present in the now-fallen people and animals of the earth. Again, cutting-edge genome research confirms the Genesis account of origins.”If the devil’s in the perturbed cell type division, what led to the division in the first cell with DNA that replicated sans the pathology?For fun, let’s see what the trolls claim about that.
3) Excerpt: “…they used a super-resolution microscope at USC that generates 3-D images of objects at the nanometer scale, to examine the damage structures in crisp detail.”
Is this “word play?” My first impression links it from the CRISPR-Cas9 technology to 3-D protein folding that is perturbed by viruses. The “crisp” details and “3-D” imagery may be the key to understanding the devil is in the details of perturbed RNA-mediated cell type differentiation.See also: A 3D Map of the Human Genome at Kilobase Resolution Reveals Principles of Chromatin Looping
4) I’ll try to keep this simple and cite Wikipedia.
“The common function of helicases accounts for the fact that they display a certain degree of amino acid sequence homology; they all possess sequence motifs located in the interior of their primary structure, involved in ATP binding, ATP hydrolysis and translocation along the nucleic acid substrate. The variable portion of the amino acid sequence is related to the specific features of each helicase.The presence of these helicase motifs allows putative helicase activity to be attributed to a given protein, but does not necessarily confirm it as an active helicase. Conserved motifs do, however, support an evolutionary homology among enzymes.”
If you can link stress from metabolic networks to dysfunctional chromosomal rearrangements via mutations in genetic networks, you can probably link the lack of stress to ecological speciation. If not, there’s a model for that!
5) Where are the trolls who support the claims of PZ Myers that include his claim that I am a crank?

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