Posted on August 11, 2014 by James Kohl.As Animals Mingle, a Baffling Genetic Barrier
A short stretch of DNA is challenging what it means to be a species.
August 5, 2014
Excerpt: “Scientists have dubbed such regions of the genome “islands of speciation.” The persistence of such islands is a phenomenon that has been observed in a variety of organisms. Natural selection appears to put evolutionary pressure on these regions, which keeps both the genes and their corresponding traits distinct even in the face of interbreeding, while the rest of the genome can mix.”
My comment: Estrogen receptor α polymorphism in a species with alternative behavioral phenotypes details what appears to lie at the origin of species diversity in species from microbes to man in the context of these “islands of speciation.”
In their supporting information, the authors state: “The ZAL2 and ZAL2m alleles code for 597 amino acids, with two fixed differences driving a Val73Ile and Ala552Thr polymorphism in ZAL2m.” This links differences in parental feeding to nutrient-dependent pheromone-controlled amino acid substitutions that differentiate the cell types of all cells in all individuals of all species via conserved molecular mechanisms. Amino acid substitutions allow “islands of speciation” to emerge in the context of stabilized protein folding that is required for DNA to organize the genomes of what have consistently been referred to as different species.
For example, in the mouse-to-human model of cell type differentiation a valine to alanine substitution (similar to the one in the sparrows) differentiates the cell types of hair, teeth, sweat glands, and mammary tissue. See: Modeling Recent Human Evolution in Mice by Expression of a Selected EDAR Variant
However, when placed in to the context of chromosomal rearrangements in vertebrates, cause and effect is divorced from theories about mutation-initiated natural selection and the evolution of biodiversity. We can clearly see the differences between male mice and men, but we cannot see the similarities. Some evolutionary theorists hate to see such refutations of what they have offered as correlations based on observations and population genetics that this article politely states bastardized Darwin’s theory of evolution (with my emphasis below).
“Darwin, when he proved that species evolved, also proved there was no such thing as species,” said James Mallet….”
Population geneticists needed to show that species somehow evolved so they invented a theory of mutation-initiated natural selection and defined their terms before anyone realized that ecological variation leads to …
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Posted on August 11, 2014 by James Kohl.CRISPR Corrects Blood Disorder Gene
Scientists use the genome-editing technique to fix a disease-causing mutation in human cell lines.
By Kerry Grens | August 5, 2014
Excerpt 1): “β-thalassemia is caused by a mutation in the HBBgene, resulting in a severe hemoglobin deficiency.”
Excerpt 2): “One of the concerns with using CRISPR is that it has the potential to snip other, unintended sites in the genome.”
My comment: My concerns about using CRISPR are based on the likelihood that β-thalassemia results from nutrient-dependent amino acid substitutions that stabilize DNA in organized genomes. If so, using CRISPR will lead to genomic instability akin to using pharmaceuticals that alter protein folding and cell type differentiation that is nutrient-dependent and pheromone-controlled.
My comment to The Scientist appears below:
1) “The hemoglobinopathies, or Hb variants, are attributable to amino acid substitution(s) in either globin chain. Currently, 1,179 total hemoglobin variants have been characterized.2″
2)”Countries with the highest incidence of diabetes also tend to have high incidence of Hb variants in the population.14”
Correlations (don’t say it*) between amino acid substitutions that appear to differentiate the cell types of all cells in all individuals of all different species suggest the amino acid substitutions that differentiate cell types with hemoglobin variants and those that somehow contribute to diabetes also are nutrient-dependent.
However, the amino acid substitutions are not likely to become fixed in the absence of their effect on DNA stability in the organized genomes of species with circulatory systems that also produce pheromones, which control the physiology of reproduction in species from microbes to man.
For examples of other correlations in species with and without circulatory systems see: Nutrient-dependent/pheromone-controlled adaptive evolution: a model.
Is there a model of mutation-caused cell type differentiation via amino acid substitutions in species from yeasts to mammals? If not, my model may be the only model of biophysically-constrained biologically-based cause and effect that can be compared to correlations provided in the context of theories about how mutations and natural selection somehow led to the evolution of biodiversity.
* Don’t say that correlations are not causation unless you first attest to the fact that you have never thought in terms of Mutation-driven evolution without recognizing your unstated belief that correlations must be causation. If not, the theories about mutaitions are not biologically plausible theories.…
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Posted on August 11, 2014 by James Kohl.
Serbian government honored me by putting me on their 20 recently
In the context of nutritional epigenetics and “fitness,” small RNAs are clearly the drivers of ecological adaptations, which are globally manifested in affects on behavior associated with purchasing power.
Amir Siddiqui is an expert on fitness.
However, his size does not seem to matter in the context of biologically-based cause and effect linked from nutrition to epigenetic effects on hormones that affect behavior.
At the macroscopic level, appearances can be deceiving, even the appearance of faces on currency.
Amir Siddiqui is obviously big and healthy. But he may also know what others must remember. Nutrient-dependent microRNAs are the cause of everything, including our desire to eat more cheesecake (e.g., one of Amir’s favorites).
That fact was recently supported by experimental evidence reported as “The splicing modifiers reported here are orally bioavailable compounds that penetrate into all of the tissues we tested—including brain, spinal cord, and muscle—and consequently exert their action on SMN2 splicing in all cells of the body.” See:SMN2 splicing modifiers improve motor function and longevity in mice with spinal muscular atrophy
Few others may understand what that means, but Amir exemplifies it. Across-species examples from model organisms are required. With examples they can see, others may better understand how the decisions we make about what to eat lead to nutrient-dependent changes in the microRNA/messenger RNA balance. Those changes lead from ecological variation to the amino acid substitutions that differentiate our cell types via the conserved molecular mechanisms that differentiate all the cell types of all individuals of all species from microbes to man.
Amir has a great sense of humor and his sense of humor is also an example of how people need not know anything about biophysical constraints and molecular mechanisms to understand what is obvious about nutritional epigenetics. We are what we eat!…
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Posted on August 9, 2014 by James Kohl.Geneticists decry book on race and evolution
Excerpt 1): ‘…geneticists have crafted a joint response, concluding that “there is no support from the field of population genetics for Wade’s conjectures.”
Excerpt 2): “…Wade charged that his critics were “indoctrinated in the social-science creed that prohibits any role for evolution in human affairs” and contended that the book’s central argument “has not been challenged by any serious scientist.”
My comment: Dobzhansky’s claims seem to be relevant.
From 1964 “…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!” http://icb.oxfordjournals.org/…
Are population geneticists “serious scientists?”
From 1973 “…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.” http://www.jstor.org/stable/44…
Do population geneticists know the difference that a single amino acid substitution makes?
See also: Natural Selection Promotes Antigenic Evolvability “…no mutational mechanism that is biased toward amino acid substitutions has been described.”http://dx.doi.org/10.1371%2Fjo…
Do population geneticists know how cell type differentiation occurs in species from microbes to man?
Until a mutational mechanism is discovered that might possibly somehow link mutation-initiated natural selection to the evolution of biodiversity, all we have to explain biophysically-constrained biologically-based biologically plausible cause and effect is facts. Have the facts been considered by population geneticists in the context of Darwin’s ecological approach to biodiversity: his ‘conditions of life?’
If Dobzhansky’s amino acid substitutions are nutrient-dependent (a fact?) and the physiology of reproduction is pheromone-controlled (a fact?), amino acid substitutions link Darwin’s ‘conditions of life’ from the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man via conserved molecular mechanisms.
The obvious link is from ecological variation (e.g., nutrient availability) to pheromone-controlled nutrient-dependent ecological adaptations. The adaptations are manifested in the morphological and behavioral phenotypes of all species in the context of reproduction that leads to nutrient-dependent amino acid substitutions and cell type differentiation. Cell type differentiation leads to biodiversity (e.g., without the pseudoscientific nonsense added to Darwin’s theory by population geneticists).
Finding support from population geneticists for the denigration of Wade’s approach is the politically correct, albeit academically irresponsible path of least resistance. Finding support from molecular biologists is unlikely because few are willing to become involved in any issue of racial …
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Posted on August 8, 2014 by James Kohl.Pregnancy Stress Spans Generations
The stressors a female rat experiences during pregnancy can have repercussions for her granddaughters, a study shows.
By Anna Azvolinsky | August 7, 2014
Excerpt: “These changes could be the result of a microRNA (miRNA)-mediated mechanism, which may be epigenetically inherited across generations.”
There is currently no alternative explanation for these changes. However, a model of how nutrient-dependent pheromone-controlled amino acid substitutions link cell type differentiation (e.g., from the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man via conserved molecular mechanisms) explains how nutrient-dependent changes in the microRNA/messenger RNA balance cause effects on hormone-organized behaviors that also are affected by hormones.
Yes, it’s complicated! However, the link from ‘effect’ to ‘affect’ was explained in Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Bruce McEwen also focussed on the difference between ‘effect’ and ‘affect’ in a correction to Brain on stress: How the social environment gets under the skin
Simply put, evolutionary theorists must realize that ecological variation and nutrient uptake are required for changes to the microRNA/messenger RNA balance. Those changes result in cell type differentiation via amino acid substitutions, which stabilize DNA in organized genomes. Until evolutionary theorists begin to think in terms of biophysically-constrained protein folding, they may continue to tout the pseudoscientific nonsense of mutation-initiated natural selection and the evolution of biodiversity.
Fortunately, serious scientists know that mutations perturb protein-folding, which means that mutations do not stabilize DNA in organized genomes. That’s why mutations cannot be linked from ecological variation to epigenetic effects on hormones that affect behavior manifested in increasing organismal complexity associated with morphological phenotypes.
Clearly, the evolutionary theorists can explain differences in morphological phenotypes that arise from mutations. But the fact that they cannot explain how mutations could effect hormones, which affect behavior, leaves some serious scientists wondering.
In the early 1990s, I began to wonder why the theorists were unable to think in terms of olfactory/pheromonal input, which we now know epigenetically effects hormones that obviously link ecological variation to ecological adaptations via affects on behavior. Recently, it has become clearer that evolutionary theorists cannot think about anything outside the context of mutation-initiated natural selection and the evolution of biodiversity. Some of them are even attempting to re-invent their theories using the term “epimutation.”
I hope that serious scientists will stop …
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