Energy-dependent RNA methylation (8)

By: James V. Kohl | Published on: June 9, 2016

Multiplexing Genetic and Nucleosome Positioning Codes: A Computational Approach

Mutation Monte Carlo method (MMC):
Excerpt:

The mutation moves change the bp sequence but keep the DNA configuration fixed. Both moves change the energy, Eq (1), of the two bp steps involved.

My comment: Moves that change energy cost energy. Attributing energy-dependent changes in base pairs to mutations without linking them to the source of the energy change is a neo-Darwinian trick.
Nucleosome-amino acid correlation analysis:
Excerpt:

This produces occurrence probabilities of codons (or trinucleotides) along nucleosomes. All synonymous codons (or corresponding trinucleotides) are then lumped together, resulting in probability distributions of “amino acids” along nucleosomes that reflect their preferred rotational settings.

My comment: Their first trick forces them to use probability distributions of “amino acids” instead of using nutrient energy-dependent changes in hydrogen-atom transfer in DNA base pairs in solution to link all biodiversity via the innate immune system, the de novo creation of G protein-coupled receptors, and supercoiled DNA, which protects all organized genomes from virus-driven energy theft.
That’s how two tricks are commonly used by theorists to link virus-driven energy theft from mutations to all pathology without linking fixation of energy-dependent RNA-mediated amino acid substitutions to all healthy longevity via the physiology of reproduction.
Their computer model supports all the claims about energy-dependent cell type differentiation that have ever been made by serious scientists and their conclusion refutes all the ridiculous claims neo-Darwinian theorists have made about evolution. Their conclusion tells the rest of the story:
Conclusion:

It will be interesting to study whether well-positioned nucleosomes with special properties reflecting their genomic context have also emerged through a mechanical evolution.

My comment:  Simply put, these theorists want more money to be wasted on attempts to link bioinformatics from energy-dependent changes to emergence and attempts to link emergence to the evolution of all biodiversity outside the context of what is known about energy as information.
Reported as: Second layer of information in DNA confirmed
Excerpt:

….evolutionary changes in DNA—mutations—that have two very different effects: The letter sequence encoding for a specific protein can change, or the mechanics of the DNA structure can change, resulting in different packaging and levels of DNA accessibility, and therefore differing frequency of production of that protein.

My comment: The claim that evolutionary changes in DNA are mutations with different effects is based on misrepresentations like these.

Mutation is the change of genomic structure and includes nucleotide substitution, insertion/deletion, segmental gene duplication, genomic duplication, changes in gene regulatory systems, transposition of genes, horizontal gene transfer, etc. (2) Natural selection is for saving advantageous mutations and eliminating harmful mutations. Selective advantage of the mutation is determined by the type of DNA change, and therefore natural selection is an evolutionary process initiated by mutation. It does not have any creative power in contrast to the statements made by some authors.  (p . 196)

For comparison, see: From Fertilization to Adult Sexual Behavior

The Genome, positioning, timings. There are major structural differences between the X and Y chromosomes; e.g., centromeric aiphoid repeats sequences and distribution of heterochromatin (Graves, 1995; Wolfe et al., 1985). These structural differences correlate with sexually dimorphic chromosomal positioning within the nucleus and with male/female differences in replication timing of the active X, the inactive X, and the Y chromosomes, e.g., Boggs and Chinault (1994), Clemson and Lawrence (1996); Hansen, Canfield, and Gartler (1995). Increasingly the structure and timings within the nucleus are realized as contributing to gene expression regulation (Manders, Stap, Strackee, van Driel, and Aten, 1996; Stein, Stein, Lian, van Wijnen, and Montecino, 1996).
Molecular distance. As measured in centimorgans, human and other species’ male and female chromosomes, including the autosomes, tend to have different lengths in various segments. To some extent, this suggests a correlation with physical distance but instead the differing lengths are based upon rates of recombination; although sections of most female chromosomes are longer than their homologous counterparts in male chromosomes, in some segments of various chromosomes opposite length-difference occurs, with males having larger centimorgan values than females in those regions (Lawrence, Collins, Keats, Hulten, and Morton, 1993; Murray, Buetow, Weber, Ludwigsen, Scherpbier-Heddema, Manion, Quillen, Sheffield, Sunden, and Duyk, 1994; Straub, Speer, Luo, Rojas, Overhauser, Ott, and Gilliam, 1993). While ramifications of these centimorgan sexual dimorphisms are not yet clearly established, in recent years cis- and trans-acting factors contributing to these recombination length differences have been reported for a specific part of the murine major histocompatibility complex (MHC) (Shiroishi, Sagai, Hanzawa, Gotoh, and Moriwaki, 1991).
Molecular epigenetics. It is now understood that certain genes undergo a process called “genomic or parental imprinting.” Early in embryonic development attached methyl groups become removed from most genes. Several days later, methyl groups are reattached in appropriate sites. Fascinatingly, some such genes reestablish methylation patterns based upon whether the chromosomal segment carrying the gene came from maternal or paternal chromosomes. These sexually dimorphic patterns are labeled genomic or parental imprinting, and these imprintings are inheritable but non-genetic modifications of specific genes (Razin and Shemer, 1995; Reik, 1989; Surani, 1991; Zuccotti and Monk, 1995).

My comment: All of the differences mentioned above are nutrient energy-dependent and they link what was reported as “Second layer of information in DNA confirmed” to all extant biodiversity via what is now known about RNA methylation and RNA-directed DNA methylation and how virus-driven energy theft is linked to all pathology. Simply put, serious scientists have already linked information as energy from energy-dependent changes in angstroms to ecosystems in all living genera. But obviously, the serious scientists need more money to continue Combating Evolution to Fight Disease.
I’ve recommended that more funding be used to support serious scientists and that funding for support of the evolution industry be discontinued. Serious scientists will continue to use what is known about the two epigenetic traps that link the sun’s biological virucidal energy to the de novo creation of nucleic acids and the de novo creation of receptors that allow nutrients to enter cells. Pseudoscientists may continue to use tricks in attempt to confuse others about the obvious need to link top-down causation to biologically-based cause and effect by models that are not merely based on calculations. But the tricks are becoming quite clear.
See for comparison: 

…genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world. In this view of evolution there is no need of considering teleological elements (p. 199).

My comment: Has any serious scientist ever claimed “…there is no need of considering teleological elements” in the context of their view of evolution?


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