RNA-mediated theory killers (11) (12) (13) (14) (15)

By: James V. Kohl | Published on: January 6, 2016

Historical perspective

Scent of a Book Deal (1995)

Excerpt:

The search for love the second time around can sometimes lead to scientific as well as romantic inspiration. At least, that’s what happened to James Vaughn Kohl, coauthor of the recently published volume The Scent of Eros (New York, Continuum Publishing Co., 1995). In a press release accompanying the book, Kohl-who manages a clinical laboratory for a group of physicians at Partell Medical Center in Las Vegas-writes, “My scientific interest in the nature and nurture of human sexuality dates back more than 10 years to a change in my attitude toward sexuality-one that came about as a result of a failed marriage.” The search for an “explanation for either my ex-wife’s or my own newly acquired sexual behavior” led Kohl to study the link between odors and pheromones, or sex attractants. The book, which Kohl wrote with Robert T. Francoeur, a professor of human sexuality at Farleigh Dickinson and New York universities, explains that odors can accelerate puberty, control women’s menstrual cycles, and influence sexual orientation.

My comment: Like every other aspect of morphological and behavioral development during life history transitions, puberty, menstrual cycles, and sexual orientation are RNA-mediated events.

RNA-mediated theory killers

(11) Epigenetic Alterations Determine Ant Behavior

Excerpt:

Tweaking the proteins that control how tightly DNA is wound can dramatically alter behavior in Florida carpenter ant workers…

My comment: Use of the ant model organism as a proxy for what has been detailed in the context of the honeybee model organism is an interesting distraction. Here is what has been known about RNA-mediated cell type differentiation in all vertebrates and invertebrates since the mid-1990s.
See: Nutrient-dependent/pheromone-controlled adaptive evolution: a model
Excerpt:

Nutrient-dependent pheromone-controlled reproduction underlies what is common (Locasale, 2012) to all models of natural selection, sexual selection, and species diversity (Frady, Palmer, & Kristan, 2012). Animal models are often used to model human physical and mental disorders. The honeybee already serves as a model organism for studying human immunity, disease resistance, allergic reaction, circadian rhythms, antibiotic resistance, the development of the brain and behavior, mental health, longevity, diseases of the X chromosome, learning and memory, as well as conditioned responses to sensory stimuli (Kohl, 2012).

See also:  Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors.
Excerpt:

Conditioned hormonal and behavioral responses to odors associated with food selection and conspecifics in mammals require something like the collective ‘neural networks’ of beehives. Philosophically and metaphorically, these neural networks extend to mammalian brains. The concept that is extended is the epigenetic tweaking of immense gene networks in ‘superorganisms’ (Lockett, Kucharski, & Maleszka, 2012) that ‘solve problems through the exchange and the selective cancellation and modification of signals (Bear, 2004, p. 330)’. It is now clearer how an environmental drive probably evolved from that of food ingestion in unicellular organisms to that of socialization in insects. It is also clear that, in mammals, food odors and pheromones cause changes in hormones such as LH, which has developmental affects on sexual behavior in nutrient-dependent, reproductively fit individuals across species of vertebrates.

(12) RNA Epigenetics

Excerpt:

Modifications to RNA molecules are much more common and are critical for regulating diverse biological processes.

My comment: Is it not yet perfectly clear that ecological variation links atoms to ecosystems via the ability of nutrient energy-dependent microRNAs and adhesion proteins to stabilize organized genomes in the context of the supercoiled DNA that protects all living genera from virus-driven genomic entropy?
Nothing currently known about biophysically constrained RNA-mediated protein folding chemistry during thermodynamic cycles of protein biosynthesis and degradation has changed.  When will everyone simply admit that Dobzhansky (1973) was correct when he reported that:

…the so-called alpha chains of hemoglobin have identical sequences of amino acids in man and the chimpanzee, but they differ in a single amino acid (out of 141) in the gorilla. ( p. 127)

Are serious scientists trying to be polite when they destroy all the claims of neo-Darwinian theorists by doing it gradually?

(13) Estimating Information Processing in a Memory System: The Utility of Meta-analytic Methods for Genetics

Abstract Excerpt:

Systematic review was used to identify behavioral experiments examining the physiological basis of olfactory memory and meta-analytic approaches were applied to assess the role of lobular specialization. Multivariate meta-regression models revealed that short-term memory lobular specialization is not supported by the data; it identified the cellular extent of a transgenic driver as the major predictor of its effect on short-term memory. These findings demonstrate that effect sizes, meta-analysis, meta-regression, hierarchical models and estimation methods in general can be successfully harnessed to identify knowledge gaps, synthesize divergent results, accommodate heterogeneous experimental design and quantify genetic mechanisms.

Reported as: Meta-Research: Why we should care.
Excerpt: 

Meta-analysis, often thought of as a tool for combining clinical and preclinical trial data (as in the example just mentioned), can be just as powerful in basic science, as seen in this PLOS Genetics meta-analysis of behavioural studies in fruit fly mutants, wresting statistically significant results from studies that are themselves individually marginal.

My comment: The meta-analysis is readily linked to what was known about nutrient-dependent pheromone-controlled ecological adaptayion in flies when Dobzhansky reported it in 1972.
Excerpt:

Reproductive isolation evidently can arise with little or no morphological differentiation. (p. 665)

My comment: No one I know seems willing to put that claim into the context of what is currently known about the links from atoms to ecosystems that clearly show reproductive isolation arises in the context of RNA-mediated events linked to chromosomal rearrangements. Is anyone you known willing to attempt to put any claim that Dobzhansky ever made into any current current perspective on random mutations and evolution of differences in flies or any other model organism?
Only one biologically uninformed science idiot has done that for nearly two years after I responded to his attack on my accurate representations of biologically-based cause and effect, which I supported with evidence from a study of white-throated sparrows.
See: One crank dies, another rises to take his place
Behold James Vaughn Kohl.

Ecological adaptation occurs via the epigenetic effects of nutrients on alternative splicings of pre-mRNA which result in amino acid substitutions that differentiate all cell types of all individuals of all species. The control of the differences in cell types occurs via the metabolism of the nutrients to chemical signals that control the physiology of reproduction.
These facts do not refute evolution; they simply refute the ridiculous theory of mutation-initiated natural selection that most people here were taught to believe is the theory of evolution.
That theory is far too ridiculous to be anything but a joke in the context of biological-based increasing organismal complexity. But here, we have lots of jokers, don’t we? The proof of ecological variation that appears to refute the theory of evolution, which actually refutes itself, is that ecological adaptations occur too fast for mutations to compete with them as a source of anything but diseases and disorders.

My comment: The atoms to ecosystems links from viruses to pathology have since been established in the context of everything known to serious scientists about physics, chemistry, and the conserved molecular mechanisms of biophysically constrained RNA-mediated protein folding chemistry that links supercoiled DNA to protection against virus-driven genomic entropy. I placed the following two cited works into the context of the discussion

Roles of Mutation and Selection in Speciation: From Hugo de Vries to the Modern Genomic Era

Excerpt:
…population geneticists such as Wright (1941) showed that the probability of fixation of these chromosomal rearrangements is so low that they would not be easily established in the population unless population size is very small (say less than 10). For this reason, the idea that new species are formed by chromosomal rearrangements was almost abandoned.
Almost abandoned? PZ Myers called Davison a “crank” for encouraging discussion of that idea, which has since been fully supported by experimental evidence. Why does an atheistic biology teacher want others to think that someone else is a crank because that person doesn’t agree with the ridiculous idea of mutation-driven evolution?

Estrogen receptor α polymorphism in a species with alternative behavioral phenotypes

Excerpt (with my emphasis)

The evolution of behavior relies on changes at the level of the genome; yet the ability to attribute a behavioral change to a specific, naturally occurring genetic change is rare in vertebrates. In the white-throated sparrow (Zonotrichia albicollis), a chromosomal polymorphism (ZAL2/2m) is known to segregate with a behavioral phenotype. Individuals with the ZAL2m haplotype engage in more territorial aggression and less parental behavior than individuals without it. These behaviors are thought to be mediated by sensitivity to sex steroids, and the chromosomal rearrangement underlying the polymorphism has captured a prime candidate gene: estrogen receptor 1 (ESR1), which encodes estrogen receptor α (ERα). We therefore hypothesized that the behavioral effects of the ZAL2m rearrangement are mediated by polymorphism in ESR1. We report here that (i) the ESR1 promoter region contains fixed polymorphisms distinguishing the ZAL2m and ZAL2 alleles; (ii); those polymorphisms regulate transcription efficiency in vitro and therefore potentially do the same in vivo (iii); the local expression of ERα in the brain depends strongly on genotype in a free-living population; and (iv) ERα expression in the medial amygdala and medial preoptic area may fully mediate the effects of genotype on territorial aggression and parenting, respectively. Thus, our study provides a rare glimpse of how a chromosomal polymorphism has affected the brain and social behavior in a vertebrate. Our results suggest that in this species, differentiation of ESR1 has played a causal role in the evolution of phenotypes with alternative life-history strategies.

(14) Determination of the Spontaneous Mutation Frequency of Ebola virus and Exploitation of this Therapeutically

Excerpt:

Typically, RNA viruses have high spontaneous mutation rates due to error prone RNA-dependent RNA polymerases. However, it is unknown if filoviruses exhibit a high spontaneous mutation rate (3, 4). It had been thought that EBOV did not evolve in the context of a single outbreak (4) but recent data from the West African outbreak suggest that there is evolution (5-8). Filoviruses have a wide host range and show great potential for emergence: to new geographic regions, to new hosts, and by new modes of transmission (9-15). Information about mutation frequencies in filoviruses could help lead to a better understanding of these topics. Furthermore, from the current outbreak we are learning the importance of how the virus changes and how this could impact future diagnostics, treatments, and preventative measures (6-8).

Reported as: Study shows high frequency of spontaneous mutation in Ebola virus
Excerpt:

Any change in a genome can be neutral, negative, or positive to a virus,” Griffiths explained. He added that “interestingly, viruses appear to have evolved to have an optimal mutation rate. Increasing the mutation rate could produce a negative effect on the virus and serve as a valuable therapeutic tool.

My comment: Viruses do not evolve. They adapt by stealing energy from cells. The major antigenic changes of the influenza virus are primarily caused by a single amino acid near the receptor binding site. Neo-Darwinists changed their claims about evolution to include anything that caused a change in the genome. All serious scientists still refuse to use de Vries definition of mutation and the neo-Darwinists assumptions about the time it might take for one species to evolve from another.
But some researchers still try to frame their results in the context of “change over time.” They report results in the terms only theorists have used to make it appear that they do not know anything more than a pseudoscientists. And then they laugh at the pseudoscientists, usually behind their backs. But sometimes in parodies like this one. They know the pseudoscientists won’t get their jokes, and they can keep laughing at the neo-Darwinists by claiming “We tried to tell them they knew nothing about cell type differentiation.”

(15) Retracted a Few Years Later

Excerpt:

A separate set of researchers said in a letter appearing in Nature that same year that it had analyzed data from the original paper and uncovered “features that are inconsistent with the known physical properties of macromolecular structures and their diffraction data” and questioned the first paper’s findings.

My comment: The features that are inconsistent with the known physical properties of macromolecular structures may include any that do not link atoms to ecosystems in the context of what is currently known about biophysically constrained nutrient energy-dependent protein folding biochemistry and RNA-mediated DNA repair.


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