poster-from-jesse

Are evolutionary theorists 'nob ends'?

Interview – Prof Brian Cox and Robin Ince

Robin Ince “Am I wrong to sometimes be scared of science idiots?”

Brian Cox  “…my favoured response would be: ‘you bunch of utter nob ends’.

 See also:  “The problem with today’s world is that everyone believes they have the right to express their opinion AND have others listen to it. The correct statement of individual rights is that everyone has the right to an opinion, but crucially, that opinion can be roundly ignored and even made fun of, particularly if it is demonstrably nonsense!”– Brian Cox

James Kohl shared The Skeptics’ Guide to the Universe‘s photo.

“[W]hat Haldane, Fisher, Sewell Wright, Hardy, Weinberg et al. did was invent…. The anglophone tradition was taught. I was taught, and so were my contemporaries, and so were the younger scientists. Evolution was defined as “changes in gene frequencies in natural populations.” The accumulation of genetic mutations was touted to be enough to change one species to another…. No, it wasn’t dishonesty. I think it was wish fulfillment and social momentum. Assumptions, made but not verified, were taught as fact.”
That’s nonsense! See for comparison:
1) Whole-exome sequencing identifies a de novo TUBA1A mutation in a patient with sporadic malformations of cortical development: a case report “We successfully identified a causative TUBA1A mutation in a patient with sporadic MCD associated with a simplified gyral pattern by using whole-exome sequencing. The identified novel mutation (E27Q) was located in the N-terminal region of the amino acid sequence. Rapid and comprehensive mutation analysis by using whole-exome sequencing may be useful for genetic counseling in sporadic cases of human disorders derived from multiple candidate genes.” My comment: Mutations cause diseases.
2) Exome sequencing and subsequent association studies identify five amino acid-altering variants influencing human height. Excerpt: “This study demonstrated the utility of next-generation sequencing in identifying genetic variants and loci associated with complex traits.” My comment: Increasing organismal complexity arises via amino acid substitutions that stabilize the organized genome.
3) Exome RNA sequencing reveals rare and novel alternative transcripts Excerpt: “…we propose that ExomeRNAseq may be an excellent approach for cross-species comparisons. It was recently shown that exome capture on DNA can efficiently be used to map variation across primates (24,25), and it should work equally well for RNA based capture. Since we show that we can find a large number of coding variants in the data, exome enrichment at the level of RNA can be used both for annotation of gene models and identification of variation.” My comment: ExomeRNAseq reveals the involvement of RNA-mediated events that link amino acid substitutions to increasing organismal complexity. See also: “…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.” Dobzhansky (1973)

4) Molecular indexing enables quantitative targeted RNA sequencing and reveals poor efficiencies in standard library preparations Excerpt: “RNA sequencing (RNA-Seq) is a powerful method for the measurement of global gene expression (1, 2). As a discovery tool, the method has dramatically increased our knowledge of the transcriptome, providing new insights into transcript diversity, including the discovery of new structural variants such as alternative splicing, gene fusions or rearrangements, and low-expressed molecules.” My comment:  “Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to…” — from the ‘molecular epigenetics’ section of our 1996 review.

5) Genetic mutation Excerpt: ” …mutations provide the “raw material” upon which the mechanisms of natural selection can act.” My comment: I cannot imagine a more ridiculous statement of cause and effect. But remember: “…everyone has the right to an opinion, but crucially, that opinion can be roundly ignored and even made fun of, particularly if it is demonstrably nonsense!”– Brian Cox

6) For comparison, see: Nutrient-dependent/pheromone-controlled adaptive evolution: a model. Excerpt: “This model details how chemical ecology drives adaptive evolution via: (1) ecological niche construction, (2) social niche construction, (3) neurogenic niche construction, and (4) socio-cognitive niche construction. This model exemplifies the epigenetic effects of olfactory/pheromonal conditioning, which alters genetically predisposed, nutrient-dependent, hormone-driven mammalian behavior and choices for pheromones that control reproduction via their effects on luteinizing hormone (LH) and systems biology.”
My comment: My model links what is currently known about physics, chemistry, and conserved molecular mechanisms, which link the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man. I include aspects of RNA-directed DNA methylation in model organisms and provide examples of RNA-mediated events that link amino acid substitutions to cell type differentiation in all cells of all individuals and all tissues in all organs of all organ systems in all organisms that exemplify increasing organismal complexity.
For comparison, evolutionary theorists seem to believe in the pseudoscientific nonsense about mutation-driven evolution. “In other words, 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)

Teleological argument A teleological or physico-theological argument, also known as an argument from design, is an argument for the existence of God or, more generally, for an intelligent creator “based on perceived evidence of deliberate design in the natural or physical world”.[1]

Please join me and others as we ignore and even made fun of the demonstrable nonsense touted by evolutionary theorists. It’s time for serious scientists to move forward by linking the present to the past via what is known about amino acid substitutions that differentiate the cell types of all cells in all individuals of all species from microbes to man. Thus, the question also arises: Are human ethologists ‘nob ends’? See for example, Jay R. Feierman who is the moderator of the human ethology yahoo group.  He wrote:

On 11/1/12: “Random mutations are the substrates upon which directional natural selection acts.
On 2/16/13 : “Random gene mutation is the variance generator upon which natural selection operates.
On 2/23/13: “…random genetic mutations generate the substrate upon which natural selection can act. Random genetic mutations create structural variations in protein enzymes…

 I wonder if Brian Cox also thinks Feierman is a ‘nob end.’ Similarly, is Robin Ince wrong to be scared of science idiots, like Feierman.

Others should begin to fear all science idiots and/or each ‘nob end’ who is currently attempting to manage an RNA-mediated crisis. For example, some researchers seem to think the Ebola viruses mutate and automagically change the biophysically-constrained properties of their chemical bonds. Supposedly, that’s how mutations in viruses enable changes in virulence, which actually arise via amino acid substitutions and changes in hydrogen bonds that link atoms to ecosystems. As people interact among the ecosystems of remote areas in West Africa, they will encounter more viruses that have adapted to their ecosystems. When people cannot adapt to the new viruses as quickly as the viruses adapt to the ecosystems of vitamin-deficient or undernourished people, the recipe for world-wide disaster has been established in the context of what viruses do best. They adapt! Viruses do not mutate and evolve. No species on this planet has ever done that. All have adapted to ecological variation or become extinct. Thus, across all creation of all species, viruses may both predict and be responsible for the fate of all cell types including our nutrient-dependent cell types that have differentiated, not evolved, via our pheromone-controlled physiology of reproduction. Simply put, if our Creator does not intervene, evolutionary theory may lead to the physical death of us all, which will link the present to the past as yet another testament of who is in control of all outcomes.

The concept that viruses might play a fundamental role in the evolution of the complexity of cellular life, as here proposed, may seem novel to many, especially to evolutionary biologists.” There’s a reason for that.  If you learnt evolutionary biology and genetics a decade or more ago you need to be aware that those debates have moved on very considerably, as has the experimental and field work on which they are based.

achiral-glycine

No understanding of biodiversity

No single explanation for biodiversity in Madagascar

Excerpt: “The study is part of a larger body of research aimed at identifying the climate, geology and other features of the environment that help bring new species of plants and animals into being in an area, and then sustain once they’re there.”
My comment: Like many studies, this one posits that new species automagically arise and are somehow sustained in ecological niches.
Excerpt: “What governs the distribution of, say, a particular group of frogs isn’t the same as what governs the distribution of a particular group of snakes,” Brown said. “A one-size-fits-all model doesn’t exist.”
My comment: Apparently, these researchers do not understand the fact that RNA-directed DNA methylation links the epigenetic landscape to the physical landscape of DNA in the organized genomes of all species via conserved molecular mechanisms that lead to ecological, social, neurogenic, and socio-cognitive niche construction manifested in increasing organismal complexity. Alternatively, they want others to believe there is no model of how nutrient-dependent pheromone-controlled biodiversity arises. For example, see: Nutrient-dependent/pheromone-controlled adaptive evolution: a model. “Minimally, this model can be compared to any other factual representations of epigenesis and epistasis for determination of the best scientific ‘fit’.” If the model is ignored, the claim can be made that one model links nutrient uptake to RNA-mediated biodiversity doesn’t exist.
Excerpt: “…each group of animals experiences its environment in a way that is unique to its life history and other biological characteristics,” Yoder said.”
Cell type differentiation in each individual of all groups of animals is nutrient-dependent. RNA-mediated events leads to amino acid substitutions that differentiate all cell types in all tissues of all organs in all organ systems that arise in the context of the pheromone-controlled physiology of reproduction that links biodiversity from ecological variation in nutrient availability to ecological adaptation via reproduction.
Abstract excerpt: A necessarily complex model to explain the biogeography of the amphibians and reptiles of Madagascar
“We conclude that patterns are influenced by a combination of diversification processes rather than by a single predominant mechanism. A ‘one-size-fits-all’ model does not exist.”
My comment: The model of nutrient-dependent pheromone-controlled RNA-mediated biodiversity has existed since 1996. It has been used to explain all biodiversity in the context of systems biology and niche construction based on details of conserved molecular epigenetics: “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…” There is no other way that cell type differentiation occurs in any cell of any species.
See also: Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors.
“Olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans (Keller et al., 2007; Kohl, 2007; Villarreal, 2009; Vosshall, Wong, & Axel, 2000).”

neuronal-plasticity

Behavioral ecology: please continue to believe in our fantasies

Behavioral ecology and genomics: new directions, or just a more detailed map?

Excerpt 1): “Transcriptome sequencing, often called RNAseq, both sequences and quantifies the portions of the genome being transcribed under conditions of interest (Wang et al. 2009; De Wit et al. 2012). Such information can be used to identify differentially expressed genes and the mutations underlying variation in gene expression and can lead to the identification of functionally important genes or suites of genes that function together (“modules”) to produce adaptive behaviors.”
Excerpt 2):  “1. Having a sequenced genome, or chromosomal region, or a transcriptome, is not necessarily helpful.”
Excerpt 3):   “4. New model systems, facilitated by the ease of obtaining genome sequences for a variety of organisms, could be extremely salutary for behavioral ecology (but see #1).”
What else can we expect from evolutionary biologists like Marlene Zuk, who have championed the role of evolution without details of an evolutionary event that links biologically-based cause and effect to increasing organismal complexity in species from microbes to man. See: Paleofantasy: What Evolution Really Tells Us about Sex, Diet, and How We Live
Excerpt: “Armed with a razor-sharp wit and brilliant, eye-opening research, Zuk takes us to the cutting edge of biology to show that evolution can work much faster than was previously realized, meaning that we are not biologically the same as our caveman ancestors.”

My comment: We cannot be biologically different than our ancestors, but Zuk and Balenger would now like others to believe two more things:
1) RNA-directed DNA methylation, which links ecological variation from amino acid substitutions to cell type differentiation and biodiversity in species from microbes to man, may be extremely beneficial in the context of behavioral ecology.
2) Use of RNA/transcription sequencing to explain how the epigenetic landscape becomes the physical landscape of DNA in the organized genomes of species from microbes to man may not necessarily be helpful.
The reality of Zuk’s claims is best expressed as RNA-mediated events explain how ecological variation leads to ecological adaptations without the pseudoscientific nonsense of mutations. Biologically-based explanations may not benefit evolutionary biologists who would rather tout pseudoscientific nonsensene about the evolution of biodiversity as they continue to misrepresent biologically-based cause and effect.
Indeed, factual representations of RNA-mediated events force evolutionary biologists like Zuk to describe evolutionary events or stop claiming
1) that evolutionary events occur and that
2) they automagically lead to the evolution of biophysically-constrained biodiversity via
3) some unknown biologically plausible mechanism that
4) is not nutrient-dependent and not pheromone-controlled.
See also: (1) An integrative analysis of DNA methylation and RNA-Seq data for human heart, kidney and liver and (2) Human pheromones: integrating neuroendocrinology and ethology.
Both reviews link what we detailed about how cell type differentiation occurs in the molecular epigenetics section of our 1996 Hormones and Behavior review: “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.”
(1): “…integrative analysis of methylation array and RNA-Seq data can be utilized to discover the global regulation of gene expression by DNA methylation and suggests that DNA methylation plays an important role in normal tissue differentiation via modulation of gene expression.”
(2) It has become obvious that the molecular mechanisms of cell type differentiation, such as alternative splicing techniques of pre-mRNA, are conserved across species and that RNA-mediated events link DNA methylation and transciptome sequencing from ecological variation to ecological adaptations in species from microbes to man. It is equally obvious that health and fitness are determined in the context of nutrient-dependent amino acid substitutions that differentiate cell types via RNA-mediated events, not via evolutionary events.
Others, like Zuk, may continue to believe in their fantasies or to claim that RNA sequencing provides nothing more than a more detailed map of evolutionary events. However, the fact that they have never described a biologically-based evolutionary event precludes use of transciptome sequencing and a detailed map of RNA-mediated events for anything other than a refutation of the pseudoscientific nonsense they have heretofore touted.
See: Genomes in turmoil: Quantification of genome dynamics in prokaryote supergenomes
Excerpt 1): “The rates of 4 types of elementary evolutionary events (hereinafter Genome Dynamics Events or GDE)…”
Excerpt 2): “Conceivably, genome dynamics is highly sensitive to local ecological factors the exact nature of which remains to be elucidated.’
My comment: Genome Dynamics Events are RNA-mediated by nutrient-uptake and pheromone-controlled physiology of reproduction. We elucidated that in From Fertilization to Adult Sexual Behavior.
What Evolution Really Tells Us about Sex, Diet, and How We Live is nothing. How we live is determined by the nutrient-dependent pheromone-controlled ecological adaptations of our ancestors, and epigenetic effects on our hormone-organized and hormone-activated behaviors. We live in the same context as our ancestors: ecological variation and ecological adaptations. We are not mutating into another species and were not naturally selected to evolve. Mutations perturb protein folding and cause disease and disorders not evolution.
 

diseases-disorders

Color vision refutes the evolutionary dogma of gene duplication

The Rainbow Connection

Color vision as we know it resulted from one fortuitous genetic event after another.

By Kerry Grens | October 1, 2014

Excerpt 1: “The fact that we have the same few amino-acid substitutions as New World monkeys argues there was a single ancestral variation that gave rise to [the cone opsins of] both Old and New World primates,” Nathans says. “It leads to an interesting twist on the evolutionary dogma of gene duplication.”
My comment: The fact that amino acid substitutions differentiate all cell types in all individuals of all species has not caused evolutionary theorists to change their claims. It has become perfectly clear that nutrient-dependent RNA-directed DNA methylation links the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man via RNA-mediated events. But theorists still seem to think in terms of mutation-initiated natural selection and the evolution of biodiversity. The fact that biodiversity is nutrient-dependent and controlled by the metabolism of nutrients to species-specific pheromones, which control the physiology of reproduction, is not considered even though evolutionary theorists have never described a biologically-based evolutionary event.
Excerpt 2: “Were it not for this little monkey and the series of genetic events that created it, we might not have the color vision we do…”
My comment: What series of genetic events created anything? Genes have no creative power; evolutionary events have no creative power.  “…natural selection is an evolutionary process initiated by mutation. It does not have any creative power…(p. 196)
Excerpt 3: “Then, an allele of one of the opsin genes mutated, producing a pigment protein that responded to previously unseen wavelengths of light.”
My comment: To my knowledge, there is no experimental evidence of biologically-based cause and effect that supports that assumption, or any of the other assumptions throughout the text of this article.
Excerpt 4: “A single nucleotide change can change your color vision.”
My comment: Is someone claiming the single nucleotide change (SNP) was caused by a mutation? Is there a model that links the SNP to color vision? The statement links changes that appear to have automagically occurred.
Excerpt 5:The results provided support for the idea that an ancient X-linked opsin gene underwent a single duplication event and that subsequent mutations in the copy shifted the absorbance spectrum of the photopigment.3
My comment: Gene duplication events are nutrient dependent. They are not caused by mutations and gene duplications or mutation-driven losses of functional genes do not lead to subsequent mutations. Nutrient-dependent gene duplication is controlled by the metabolism of the nutrients to species specific pheromones in species from microbes to man.

Facts about what is portrayed as The Rainbow Connection.

Loss of Olfactory Receptor Genes Coincides with the Acquisition of Full Trichromatic Vision in Primate That fact links RNA-directed nutrient-dependent DNA methylation and RNA-mediated events from ecological variation to amino acid substitutions and to gains and losses of protein function, which differentiate all cell types of all individuals of all species.
See for example: “…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.” Dobzhansky (1973)
RNA molecules function as the central conduit of information transfer in biology.” That fact suggests theories about how color vision arose are based on assumptions linked to the invention of neo-Darwinism via the gene-centric approach of population geneticists who knew nothing about RNA-mediated events when they began to invent their theories.
It is surprising to see those theories integrated into this article as if they suddenly had any explanatory power given what is currently known about Alternative RNA Splicing in Evolution and about Nutrient-dependent/pheromone-controlled adaptive evolution: a model.
Until recently others have made claims like “…the evolution of trichromacy as well as huge increases in social complexity have minimised the role of pheromones in the lives of primates, leading to the total inactivation of the vomeronasal system in catarrhine primates while the brain increased in size and behaviour became emancipated from hormonal regulation.” No experimental evidence of biologically-based cause and effect linked from biophysical constraints on amino acid substitutions and protein folding to cell type differentiation supports claims like that, either.
Re: “The results provided support for the idea that an ancient X-linked opsin gene underwent a single duplication event and that subsequent mutations in the copy shifted the absorbance spectrum of the photopigment.3
It’s not a good idea to suggest that the idea above has been supported by any experimental evidence that might otherwise link biologically-based cause and effect across species. First, sex differences in cell types must be explained. For example: “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…
The bottom line appears to be that people willingly accept theories about how sex differences arose and about how color vision arose because they think the theories have been supported by experimental evidence. But, the experimental evidence links ecological variation to ecological adaptations via conserved molecular mechanisms in species from microbes to man. Until biologically-based evolutionary events are described that link mutations to the amino acid substitutions that differentiate cell types associated with color vision, I hope that others will begin to examine details of RNA-mediated events that link cell type differentiation in all species from nutrient uptake to the pheromone-controlled physiology of reproduction and controlled biodiversity, which is loosely associated with color vision in: The Rainbow Connection
Close associations between frugivory in species that are blind as bats and cave fish link nutrient uptake in an atoms to ecosystems context that also links species-specific pheromones to control of cell type differentiation in the honeybee model organism and all other model organisms. Primates should not be excluded from an atoms to ecosystems model of ecological variation linked to ecological adaptations via RNA-mediated events.

human-evolution

Genomic surveillance ends our world of RNA-mediated ecological adaptations

Why is this woman smiling?

1) Identifying Recent Adaptations in Large-Scale Genomic Data

Senior author: Sabeti with co-author Rinn
Excerpt: “As natural selection can only act on mutations that drive phenotypic variation…”.

2) Genomic surveillance elucidates Ebola virus origin and transmission during the 2014 outbreak 

Senior author: Sabeti.
Excerpt: “Because many of the mutations alter protein sequences and other biologically meaningful targets, they should be monitored for impact on diagnostics, vaccines, and therapies critical to outbreak response.”

3) RNA and dynamic nuclear organization

First author Rinn.
Excerpt: “… it is becoming increasingly clear that lncRNAs are important at all levels of nuclear organization—exploiting, driving, and maintaining nuclear compartmentalization.”

4) ‘Oming in on RNA–protein interactions

First author Rinn.
Excerpt: “…the interactions between pre-mRNA and proteins fine-tune alternative splicing in a manner that can gradually create new protein functionalities without the need to create additional genes and without affecting existing proteins [4-6].”
My comment: Evolutionary theorists who think “…natural selection can only act on mutations that drive phenotypic variation…” may not realize that “…the interactions between pre-mRNA and proteins fine-tune alternative splicing in a manner that can gradually create new protein functionalities…” See our section on molecular epigenetics in 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…” (e.g., of cell types in species from yeasts to man).
Serious scientists may realize, too late, that nutrient-dependent RNA-directed DNA methylation — and pre-mRNA-mediated events that lead to mRNA-mediated amino acid substitutions — differentiate all cell types in all individuals of all living species. For example, without thinking, the non-living Ebola viruses may ecologically adapt with as little as a single amino acid substitution, like the one that differentiates all cell types of humans from chimpanzees and gorillas.
See: “…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.” Dobzhansky (1973).
What evolutionary theorists continue to think about natural selection acting on mutations that lead to the evolution of biodiversity will not matter if the Ebola viruses destroy humanity. People may ask as our species dies out: “What were the evolutionists thinking? Did they not know that Substitutions Near the Receptor Binding Site Determine Major Antigenic Change During Influenza Virus Evolution?
Did the theorists never ask: How does epistasis arise from an evolutionary process that is conceived as proceeding through the incremental accumulation of mutations?
Does any serious scientist still think that the accumulation of mutations leads to increasing organismal complexity? How could that happen?
Biophysically-constrained receptor-mediated nutrient-dependent pheromone-controlled ecological adaptations link the physiology of reproduction to behavioral phenotypes and morphological phenotypes in all living species based on the molecular mechanisms conserved in viruses.
Is there another model for that? Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems. See also: Origin of group identity: viruses, addiction and cooperation

poster-from-jesse

RNA-mediated ecological adaptation is not evolution

Prehistoric Critters Change View of Mammal Evolution

Three extinct squirrel-like species were identified from Jurassic-era fossils in China.

By Molly Sharlach | September 12, 2014

Excerpt 1): “The fossils suggest that the slender animals spent time in trees, and had hands and feet adapted for grabbing branches. Their resemblance to present-day squirrels is a result of convergent evolution, as they belong to a lineage that diverged from that of modern mammals long ago.”

My comment: Resemblance in the fossil record is meaningless, and not sufficient to attribute to convergent evolution or to estimate the time that different lineages diverged.

Excerpt 2) “Their similarity to older fossils in the group Haramiyida suggests that mammals arose more than 200 million years ago, during the Late Triassic.”
My comment to The Scientist:
Everything known about RNA-mediated events suggests and then shows via experimental evidence that ecological variation leads to ecological adaptations more quickly than neo-Darwinian theories suggest occurs via mutations and natural selection.
A single RNA-mediated nutrient-dependent amino acid substitution is all it takes for chromosomal rearrangements to rapidly lead to reproductive isolation and ecological speciation without the mutation-initiated natural selection that supposedly leads to the evolution of biodiversity via some unknown evolutionary event or events (accumulated mutations) that occurred over millions of years.
Is anyone else paying attention to facts that link interactions between pre-mRNA and proteins to the fine-tuning of alternative splicings and the de novo Creation of new functional proteins with no need to create additional genes? Guess what the de novo Creation of new proteins does without affecting existing proteins.
I’ve been guessing since 1996 (with co-authors) that the Creation of new proteins enables the chromosomal rearrangements that lead to reproductive isolation and biodiversity of morphological AND BEHAVIORAL phenotypes via nutrient-dependent pheromone-controlled RNA-mediated ecological adaptations in species from the single-celled eukaryote Oxytricha trifallax to multicellular primates (e.g, a northern white-cheeked gibbon).
Evolutionary theorists (except Dobzhansky) guessed wrong, and they should consider accepting the biological facts about RNA-mediated events in the context of ecological adaptations. It makes sense for everyone since Dobzhansky to accept the facts about amino acid substitutions. He was right about the difference one amino acid substitution makes in chimps, gorillas, and humans.
Until evolutionary theorists can describe an evolutionary event that might link the morphology AND behavior of one nutrient-dependent differentiated cell type in any individual of any species to the evolution of another nutrient-dependent differentiated cell type in an individual of another species, they should accept Dobzhansky’s Creationist views and abandon the neo-Darwinian nonsense about mutations, natural selection, and the evolution of biodiversity.
Dobzhansky had something to say about that, too. “…the only worthwhile biology is molecular biology. All else is “bird watching” or “butterfly collecting.” Bird watching and butterfly collecting are occupations manifestly unworthy of serious scientists!”

diseases-disorders

Exploding genomes and chromosomal rearrangements via RNA-mediated events

Gibbon genome and the fast karyotype evolution of small apes
This is an open access article reported as:

Gibbon genome sequence deepens understanding of primates rapid chromosomal rearrangements

Excerpt: The number of in the gibbons is remarkable, Rogers said. “It is like the genome just exploded and then was put back together,” he said. “Up until recently, it has been impossible to determine how one human chromosome could be aligned to any gibbon chromosome because there are so many rearrangements.”
My comment: Now that researchers have determined how so many chromosomal rearrangements can rapidly occur outside the context of mutations, they can link the genome of gibbons to the human genome via the following sequence of events:
1) nutrient-dependent changes in the
2) microRNA/messenger RNA balance,
3) alternative splicings of pre-mRNA, and
4) RNA-mediated events that link
5) amino acids substitutions to their fixation when they stabilize the DNA in organized genomes of species.
The nutrient-dependent chromosomal rearrangements can then be linked to the RNA-mediated stability of DNA in species from microbes to man via the conserved molecular mechanisms of reproduction isolation due to chromosomal rearrangement and species diversity due to the metabolism of nutrients to species-specific pheromones. which control the physiology of reproduction in species from microbes to man. Thus the conserved molecular mechanisms of RNA-mediated events have again eliminated any further consideration of mutations and natural selection in the evolution of biodiversity.
Until an evolutionary event is described, theorists may continue to invent and define their theories in terms that link mutated DNA to biodiversity and increasing organismal complexity that ‘just happens’ to somehow occur in explosions of chromosomal rearrangements like those that supposedly occurred during the Cambrian explosion. However, the fact that these explosions are nutrient-dependent and pheromone-controlled may mean that biodiversity arises in much less time that might otherwise be predicted in the context of pseudoscientific nonsense of population genetics and neo-Darwinism.
Note also, however, that Genome-wide DNA rearrangements are most exaggerated in ciliates, particularly in the model organism Oxytricha trifallax, which programs not only DNA deletion, but also total reorganization, through RNA-mediated events (Fang et al., 2012; Nowacki et al., 2008).
See the report here on that fact about the conserved molecular mechanisms of RNA-mediated events for comparison to unknown evolutionary events: In one of nature’s innovations, a single cell smashes and rebuilds its own genome

IMG_2329-e1413855233208-958x718

Behavior (2): All responses are RNA-mediated not genetically-determined

Diana Maria Petrosanu also asked: “who was the author of the article that had stolen your ideas?
I cannot recall claiming that anyone had stolen our ideas or my ideas.
See: Behavior: The first response is RNA-mediated not genetically-determined. In subsequent published works, I extended what we detailed about the molecular epigenetics of sex differences in cell types from yeasts to mammals via examples from model organisms of RNA-mediated cell type differentiation in different species. That is why I was surprised to see this title: The Biological Basis of Human Sexual Orientation: Is There a Role for Epigenetics?” I’ve requested a pdf reprint of the article from Dr. Vilain. I do not expect that he cited our 1996 review because I do not recall him even mentioning any works I have authored or co-authored in his publications? Is he ignoring my past publications?
For example, in our 1996 Hormones and Behavior review we (TB) wrote: “Parenthetically it is interesting to note even the yeast Saccharomyces cerevisiae has a gene-based equivalent of sexual orientation (i.e., a-factor and alpha-factor physiologies). These differences arise from different epigenetic modifications of an otherwise identical MAT locus (Runge and Zakian, 1996; Wu and Haber, 1995).”
The connection from RNA-mediated events to epigenetic modifications of the MAT locus should have been clear to any geneticist who did not know how mutations in DNA could lead to sex differences and to sexual orientation in different cell types. However, many of those who study human sexuality are like those who study evolutionary psychology. I think that is why this question was posed: Is There a Role for Epigenetics?
Anyone taught to believe an unknown evolutionary event might someday be linked to sex differences in cell types or to any and all other cell type differences in all cells of all individuals of all species has been taught to believe in pseudoscientific nonsense, and to ignore biological facts about RNA-mediated events that we (TB) detailed 18 years ago. Those who were not taught that mutations caused sex differences in cell types may have been left to wonder about how sexual orientation somehow ‘evolved.’ That’s just speculation on my part. Some people probably weren’t taught anything and never questioned the likely role of RNA-mediated events, or never questioned their teachers who probably still know nothing about molecular epigenetics and RNA-mediated events.
We wrote: “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. That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes.” (p. 337)
Was anyone taught to believe the truth about the molecular epigenetics of cell type differentiation in species from microbes to man? When I saw the question “Is there a role for epigenetics,” I decided to look more at what Eric Vilain was telling people about how sex differences in cell types arise. See, for examples:
Sex Differences in Brain and Behavior: Hormones Versus Genes
Excerpt: “We hypothesize that one central neuronal pathway establishes sexual attraction to either males or females, usually to the opposite sex. However, a variety of genetic and nongenetic biological effects might intersect this pathway (p. 260).”
My comment: In my model, the GnRH neuronal pathway establishes classically-conditioned sexual preferences in the context of epigenetically-effected RNA-mediated events via the same pathway that links food odors to experience-dependent classically-conditioned food preferences.
The genetics of sex differences in brain and behavior
Excerpt: “Altogether, there is mounting evidence for a genetic role of human sexual orientation. The overwhelming dominance of heterosexual behavior in the animal kingdom points at a tight molecular regulation of this trait.”
My comment: In my model, nutrient-dependent pheromone-controlled effects on RNA-mediated events tightly regulate the molecular epigenetics of this trait throughout the animal kingdom. That means that human sexual orientation, like the sexual orientation of sexually-differentiation cell types in yeasts is genetically predisposed. There may be mounting evidence for a genetic role of human sexual orientation, but I haven’t seen any of it. All I’ve seen is increasingly more evidence that sexual orientation is epigenetically-effected by sensory stimuli that cause RNA-mediated events.
The effects of perinatal testosterone exposure on the DNA methylome of the mouse brain are late-emerging
Excerpt: “…methylation patterns particularly during adulthood and that the emergence of sex differences in the brain may be a gradual process that is cemented over the organism’s life. Our data provide a new perspective by showing that most sex differences in CpG methylation are dynamic and not the result of acute modifications in response to hormones.”
My comment: I do not know why anyone ever thought that “…the emergence of sex differences in the brain…” was not “…a gradual process that is cemented over the organism’s life.” Attributing the sex differences to dynamic modifications but not acute modifications in hormones that organize and activate sex differences in behaviors,which obviously develop during life cycle transitions, may be the only accurate attribution Vilain has ever linked to RNA-mediated events that are epigenetically-effected by olfactory/pheromonal input that alters hormones that affect the behavior of all vertebrates and invertebrates via conserved molecular mechanisms.
My comment (from our 1996 review): 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.
Although Eric Vilain and his co-authors may think their “…data provide a new perspective…” the quote from our review should make others wonder what his group thinks is a “new perspective.”  Indeed, anyone who has followed the research on epigenetically-effected RNA-mediated events and hormones that affect behavior might wonder why anyone else ever might have thought that the RNA-mediated events did not occur across the life history transitions of species from insects to mammals.
For example, I never thought I was “Born to be Wild.” But, after I started my research on human pheromones in 1982, I gradually learned to accept the fact that my behavior was epigenetically-effected by human pheromones. From 1996 until today, I have never seen any experimental evidence of biologically-based cause and effect that links anyone’s behavior to anything that is not epigenetically-effected and RNA-mediated.
For reasons that should long ago have become obvious to all others, I am now sure that all their behavior occurs in the context of ecological variation that leads from epigenetically-effected RNA-mediated differentiation of cell types by nutrient-dependent amino acid substitutions. It is the amino acid substitutions that link behaviors manifested in ecologically adapted morphological and behavioral phenotypes to conserved molecular mechanisms in species from microbes to man.

human-evolution

Comparing divergent model organisms

Comparative analysis of the transcriptome across distant species

Excerpt: Overall, our results underscore the importance of comparing divergent model organisms to human to highlight conserved biological principles (and disentangle them from lineage-specific adaptations).
My comment: In the detailed comparisons of divergent model organisms portrayed in Nutrient-dependent/pheromone-controlled adaptive evolution: a model, I underscored what is known about cell type differentiation in species from microbes to man. By placing what is known into the context of nutrient-dependent amino acid substitutions and biodiversity controlled by the metabolism of nutrients to species-specific pheromones, I thought it would be clear that the best approach to understanding how biodiversity arose was to model it. Conclusion: “Minimally, this model can be compared to any other factual representations of epigenesis and epistasis for determination of the best scientific ‘fit’.”
The model arose from prior published works that clearly linked the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man. See for example: Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Conclusion: “Olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans…”
Now “…comparing divergent model organisms to human…” continues  “…to highlight conserved biological principles…”
These conserved biological principles are obviously the conserved molecular mechanisms of nutrient-dependent pheromone-controlled cell type differentiation we detailed in our 1996 Hormones and Behavior review article in the context of sex differences in cell types. Did anyone who is not an evolutionary theorist think that cell type differentiation occurred differently in different cells of different individuals in different species?
See for review our section on: “Molecular epigenetics” in From Fertilization to Adult Sexual Behavior
“Yet another kind of epigenetic imprinting occurs in species as diverse as yeast, Drosophila, mice, and humans and is based upon small DNA-binding proteins called “chromo domain” proteins, e.g., polycomb. These proteins affect chromatin structure, often in telomeric regions, and thereby affect transcription and silencing of various genes (Saunders, Chue, Goebl, Craig, Clark, Powers, Eissenberg, Elgin, Rothfield, and Earnshaw, 1993; Singh, Miller, Pearce, Kothary, Burton, Paro, James, and Gaunt, 1991; Trofatter, Long, Murrell, Stotler, Gusella, and Buckler, 1995). 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.”
See also: Alternative RNA Splicing in Evolution but try to think in terms of how ecological variation leads to ecological adaptations via nutrient-dependent alternative splicing of pre-mRNA. I tried to convey this message yesterday: There are no evolutionary events. There are only epigenetically-effected amino acid substitutions that differentiate cell types and pheromone-controlled cell type differentiation enables biodiversity. There is no model of how biodiversity arises via evolutionary events, because it doesn’t.

neuronal-plasticity

Order and disorder: Ecological adaptations not mutations

In the context of order and disorder that includes what is known about quantum physics and light-induced amino acid substitutions in plants and animals, as well as the control of the functional rearrangement of influenza hemagglutinin, I’m beginning to see even more confusion/obfuscation enter the picture of biophysically-constrained ecological adaptations.
The nutrient-dependent ecological adaptations are now being put into the context of mutation-initiated natural selection and the evolution of biodiversity (i.e., “Evolution for Dummies”).
ECOLOGICAL ADAPTATIONS (not mutations)
Nutrient-dependent changes in the microRNA/messenger RNA balance are readily linked from ecological variation to ecological adaptations via conserved molecular mechanisms that eliminate mutation-initiated natural selection and evolution from consideration. However, since no experimental evidence of biologically-based cause and effect has shown that mutations are ever fixed in the organized genomes of any population of any species, researchers now refer to the amino acid substitutions that are fixed in the genome as if they were epimutations (translation: epigenetically-effected mutations).
For example, in this article about epimutations, microRNAs also are referred to as small RNAs and labeled sRNAs with this mention of what a small RNA is. “Most of these sRNAs average 21–24 nucleotides in length…”
A microRNA (abbreviated miRNA) is a small non-coding RNA molecule (containing about 22 nucleotides). Thus, the quantum leap from biophysically constrainted light-induced amino acid substitutions to the nutrient-dependent microRNA/messenger RNA balance that controls genome stability via epigenetically-effected amino acid substitutions is replaced with the concept of epigenetically-effected mutations, which are called epimutuations.
By mixing the theory of mutation-initiated natural selection and the evolution of biodiversity with biological facts about how ecological variation leads to epigenetically-effected ecological adaptations manifested in biodiversity, the senior author of the “epimutations” article sets the stage for his claim to be “the first” to find something new and important.
It could be like the discovery of other molecular phenomena like introns or microRNAs, where it all began with just one example,” said Heitman. “We think this discovery may turn out to be generalized fairly quickly.
What discovery? They link nutrient-dependent microRNAs from ecological variation to ecological adaptations in the context of conserved molecular mechanisms in species from microbes to man.
The researchers think these epimutations could be employed in a variety of situations, enabling an organism to adapt to an unfavorable environment and then adapt again when conditions improve.
DISCOVER THIS!
Nutrient-dependent epigenetically-effected alternative splicings of pre-mRNA, which can be called microRNAs or sRNAs result in RNA-mediated amino acid substitutions and chromosomal rearrangements that enable organisms to adapt to ecological change. When the supply of nutrients is reduced, starvation causes experience-dependent creation of receptors that enable nutrient uptake from a novel source.
If a novel source cannot be used, the pheromone-controlled physiology of nutrient-dependent reproduction leads to death of individuals and may lead to the extinction of any species that could not ecologically adapt via experience dependent de novo creation of receptors that let nutrients into the cell. The species in which de novo creation of receptors does not occur quickly enough do not mutate into another species that was somehow naturally selected to “evolve.”
Ideas about epimutations that include what is known about sRNAs but ignore facts about the nutrient-dependent microRNA/messenger RNA balance, amino acid substitutions, and epigenetically-effected morphological and behavioral diversity will make it possible for evolutionary theorists to continue touting their nonsense about mutation-initiated natural selection until serious scientists say ENOUGH!
In the context of order and disorder, some researchers have already said this. I’m not the only one who has had ENOUGH of the pseudoscientific nonsense from population geneticists.
[W]hat Haldane, Fisher, Sewell Wright, Hardy, Weinberg et al. did was invent…. The anglophone tradition was taught. I was taught, and so were my contemporaries, and so were the younger scientists. Evolution was defined as “changes in gene frequencies in natural populations.” The accumulation of genetic mutations was touted to be enough to change one species to another…. No, it wasn’t dishonesty. I think it was wish fulfillment and social momentum. Assumptions, made but not verified, were taught as fact.
If you’ve had ENOUGH of this pseudoscientific nonsense, and want to learn more about biological facts, you may also want to learn more about why Israeli middle schools are now teaching the theory of evolution.  They appear to be using it as an example of pseudoscientific nonsense that can be compared to what is known about ecological variation and how the disorder or variation leads to well-ordered de novo creation of olfactory receptor genes via nutrient-dependent amino acid substitutions that stabilize DNA in the organized genomes of species from microbes to man.
When will other school systems begin teaching students about the differences between ridiculous theories and biological facts about biophysically-constrained ecological adaptations are manifested in biodiversity?
Earlier today I received the reprint of an article published by serious scientists in the prestigious journal Cell: Starvation-Induced Transgenerational Inheritance of Small RNAs in C. elegans. After I read more about the starvation-induced link to cell type differentiation in C. elegans, I was not surprised to see the stated goal of Oded Rechavi’s lab in Israel:

“Our principle aim in the lab is to attack scientific dogmas.”

Finally, serious scientists are no longer willing to wait for evolutionary theorists to start learning about biology. Like a few others, the Rechavi lab researchers are attacking the pseudoscientific nonsense of mutation-initiated natural selection and the evolution of biodiversity. Unfortunately, that claim went missing from the Oded Rechavi lab web page in September 2014. Perhaps it drew unwanted attention to the lab. No matter, the short perspective: RNA and dynamic nuclear organization helped to clarify the fact that “…the interactions between pre-mRNA and proteins fine-tune alternative splicing in a manner that can gradually create new protein functionalities without the need to create additional genes and without affecting existing proteins [4-6].” Clearly, the focus on RNA-mediated events and amino acid substitutions that stabilize DNA in organized genomes will lead to a future in which no serious scientist reports results in terms of mutations, natural selection, and the evolution of biodiversity.
How much clearer can it be that starving nematodes must adapt to ecological changes or their species becomes extinct. How much clearer can it be that ecological variation in the diet of nematodes is what causes nutrient-dependent amino acid substitutions that differentiate the pheromone-controlled cell types of different nematode species? In a news release published on January 13, 2013, Ralf Sommer said: “The patterns of synaptic connections perfectly mirror the fundamental differences in the feeding behaviours of P. pacificus and C. elegans.”
P. pacificus is a nematode species with teeth; C. elegans is a nematode species without teeth. The neuronal networks of the two species are wired differently and their nutrient-dependent pheromone-controlled reproduction is the most obvious cause of their differences in morphology and differences in their behavior.
No experimental evidence suggests that one species of nematode mutated into another. In fact, experimental evidence from C. elegans already has shown that mutations are not fixed in the DNA of the C. elegans organized genome. That finding “…set the stage for the development of more general theoretical models explaining the fate of new alleles…” but without fixed mutations in DNA, no model can explain the fate of new alleles in the context of natural selection that leads to the evolution of biodiversity. Mutations that are not fixed cannot be “naturally selected” and the result of the mutations cannot be evolutionary diversity.
Evolutionary theorists must invent new terms that can be used to describe how biodiversity arises, and some of them have decided to invent the term “epimutation” and attempt to explain how nutrient-dependent epigenetic changes in the organized DNA of species from microbes to man lead to the evolution of biodiversity. Shall serious scientists wish them luck with the invention of their new theories about epimutations and the evolution of biodiversity? Or will serious scientists mount an unending attack on the pseudoscientific nonsense of theorists and begin to make scientific progress that can more rapidly be made if people aren’t taught to believe in a ridiculous theory instead of biological facts about how ecological variation results in ecological adaptations? I hope that my published and unpublished works make it clear that I prefer the Rechavi lab’s attack strategy.

Nutrient-dependent/pheromone-controlled adaptive evolution: a model

and

Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems

“This atoms to ecosystems model of ecological adaptations links nutrient-dependent epigenetic effects on base pairs and amino acid substitutions to pheromone-controlled changes in the microRNA / messenger RNA balance and chromosomal rearrangements. The nutrient-dependent pheromone-controlled changes are required for the thermodynamic regulation of intracellular signaling, which enables biophysically constrained nutrient-dependent protein folding; experience-dependent receptor-mediated behaviors, and organism-level thermoregulation in ever-changing ecological niches and social niches. Nutrient-dependent pheromone-controlled ecological, social, neurogenic and socio-cognitive niche construction are manifested in increasing organismal complexity in species from microbes to man. Species diversity is a biologically-based nutrient-dependent morphological fact and species-specific pheromones control the physiology of reproduction. The reciprocal relationships of species-typical nutrient-dependent morphological and behavioral diversity are enabled by pheromone-controlled reproduction. Ecological variations and biophysically constrained natural selection of nutrients cause the behaviors that enable ecological adaptations. Species diversity is ecologically validated proof-of-concept. Ideas from population genetics, which exclude ecological factors, are integrated with an experimental evidence-based approach that establishes what is currently known. This is known: Olfactory/pheromonal input links food odors and social odors from the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man during their development.”