MicroRNAs and/or QTLs: Who buried what?

By: James V. Kohl | Published on: April 30, 2016

Making precision medicine a reality: Genomics researchers unveil road map to disease origin

Excerpt:

This study highlights the significance of mechanistic similarities for uncovering additional interacting downstream effectors of intergenic SNPs…

My comment: Use of the term QTL may limit the understanding of how energy-dependent cell type differentiation occurs and how virus-driven energy theft is linked to all pathology.
It would be great if someone would explain the difference between what QTLs do and what microRNA flanking sequences  do in the context of the molecular mechanisms of energy-dependent cell type differentiation.
Excerpt 2)

The paper, “Integrative genomics analyses unveil downstream biological effectors of disease-specific polymorphisms buried in intergenic regions,” has been identified as one of the best 30 of the year in computational biology and bioinformatics, and will be presented as a “highlight of the year” at the 2016 Intelligent Systems for Molecular Biology (ISMB) conference, the largest international conference of computational biology/bioinformatics, in July in Orlando, Fla.

My comment: Intelligent Systems? Intelligent Design? If virus-driven energy theft alters the quantitative trait loci and links angstroms to ecosystems via energy-dependent hydrogen-atom transfer in DNA base pairs in solution, will these research groups be accused of taking funds from young earth creationists who linked viruses to all pathology?

Integrative genomics analyses unveil downstream biological effectors of disease-specific polymorphisms buried in intergenic regions

Excerpt:  Fourth, we performed the enrichment analysis again using an alternate reference human genome annotation, which includes coordinates for microRNA and lncRNA (GENCODE33 version 19; best OR=25.4, P=6.4×10−6 ) to establish that our results were not the result of miscategorising SNPs within this region as intergenic (Supplementary Figure S11).
Excerpt: SNP combinations showed evidence of synergistic effects using entropy-based measures of interaction information. This result showed that SNPs engage in cooperative or epistatic effects indicative of functionally similar mechanisms.
My comment: The disease-specific polymorphisms that are buried in intergenic regions must be resurrected to cause specific diseases linked from virus-driven energy theft to failed nutrient-dependent RNA-mediated DNA repair and all pathology.
See also: What is life when it is not protected from virus driven entropy Published on 30 Mar 2016

Poster Abstract: The anti-entropic force of virucidal ultraviolet light links guanine–cytosine (G⋅C) Watson–Crick base pairing from hydrogen-atom transfer in DNA base pairs in solution to supercoiled DNA, which protects the organized genomes of all living genera from virus-driven entropy. For example, protection of DNA from permanent UV damage occurs in the context of photosynthesis and nutrient-dependent RNA-directed DNA methylation, which links RNA-mediated amino acid substitutions to DNA repair. In the context of thermodynamic cycles of protein biosynthesis and degradation, DNA repair enables the de novo creation of G protein coupled receptors (GPCRs). Olfactory receptor genes are GPCRs. The de novo creation of olfactory receptor genes links chemotaxis and phototaxis from foraging behavior to social behavior in species from microbes to humans. Foraging behavior links ecological variation to ecological adaptation in the context of this atoms to ecosystems model of biophysically constrained energy-dependent RNA-mediated protein folding chemistry. Protein folding chemistry links nutrient-dependent microRNAs from microRNA flanking sequences to energy transfer and cell type differentiation in the context of adhesion proteins, and supercoiled DNA that protects all organized genomes from virus-driven entropy.

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