Ecological adaptations and the origin of lactase persistence

March 14, 2014 | James Kohl

Genetic Origins of Lactase Persistence and the Spread of Pastoralism in Africa

Reported as:

Origins of Lactase Persistence in Africa

Large-scale sequencing effort confirms several mutations that confer lactase persistence in Africans, while haplotype analysis sheds light on the trait’s origins.

By Ashley P. Taylor | March 13, 2014

Excerpt: “Tishkoff and her colleagues identified three known variants…”

My comment: Journalists consistently report that  variants are mutations. Experimental evidence and everything currently known about conserved molecular mechanisms in species from microbes to man show that the variants are nutrient-dependent ecological adaptations.

For example, the link from fermented milk products to vitamin D-induced changes in base pairs, amino acid substitutions and epialleles that stablize the organized genome of human populations is clear. Thus, lactase persistence can be considered in the context of the hemoglobin S variant associated with endemic malaria and sickle cell disease.

Otherwise, journalists may continue to ignore what researchers know about the difference between a mutation and an ecological adaptation. Like the variants reported here, hemoglobin S is a nutrient-dependent ecological adaptation.

Variants associated with nutrient-uptake typically result in reproductive fitness, which is why they show up in different populations. Attributing reproductive fitness to mutations is confusing.

The missattribution may also cause people to think that human population-wide differences associated with skin pigmentation are due to mutations, at a time when molecular biologists realize that ecological variation and ecological adaptations are responsible for morphological and behavioral phenotypes.

Only evolutionary theorists, or those who have been taught to believe in the theory, continue to attribute ecological adaptations to mutation-driven evolution.

 

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Plasticity: Mimicry based on Darwin’s conditions of life (2)

March 11, 2014 | James Kohl

Biologists zero in on role of plasticity in evolution

Excerpt: “…were able to show that a single molecular pathway plays a role in both heritable changes in the flies’ number of ovarioles—egg-producing compartments in the ovaries—and in how they react to their environments by shutting down some ovarioles.”

See also: Insulin signalling underlies both plasticity and divergence of a reproductive trait in Drosophila

Abstract excerpt: ”This demonstrates that a plastic response conserved across animals can underlie the evolution of morphological diversity, underscoring the potential pervasiveness of plasticity as an evolutionary mechanism.”

My comment: This experimental evidence supports the claim that nutrient availability is the ecological variable that controls ecological adaptations via the metabolism of nutrients to species-specific pheromones. Effects of food “odors” and pheromones clearly link the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man via conserved molecular mechanisms. No unknown evolutionary mechanisms appear to be involved.

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

These biologists have zeroed in on the the role of plasticity in ecological adaptations.  Their experimental evidence takes us even further away from ideas about evolution that only make sense to population geneticists and their minions. Their ideas about evolution have never made sense in the light of biology.  That’s why experimental evidence continues to show that nothing about evolution makes sense in the light of molecular biology. In the light of molecular biology, ecological variation and conserved molecular mechanisms enable ecological adaptations.

In the light of molecular biology, nutrient-dependent pheromone-controlled ecological adaptations are manifested in morphological and behavioral phenotypes of species from microbes to man.

The species have not evolved. They have ecologically adapted. Species diversity exemplifies the plasticity that enables ecological adaptations. Species diversity does not exemplify evolution because the divergence of reproductive traits is nutrient-dependent and pheromone-controlled in all species. Natural selection has always been for nutrients and the metabolism of nutrients to species-specific pheromones has always enabled sexual selection in the context of the nutrient-dependent pheromone-controlled physiology of reproduction.

See also:  Mimicry based on Darwin’s conditions of life

 

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Detailed mechanisms: The puzzle of what to do next?

March 7, 2014 | James Kohl

Epigenetics: The sins of the father

The roots of inheritance may extend beyond the genome, but the mechanisms remain a puzzle by Virginia Hughes 05 March 2014

Excerpt: To many modern biologists, that’s “scary-sounding”, says Oliver Rando, a molecular biologist at the University of Massachusetts Medical School in Worcester, whose work suggests that such inheritance does indeed happen in animals3. If it is true, he says, “Why hasn’t this been obvious to all the brilliant researchers in the past hundred years of genetics?”.

My comment: Nearly all the brilliant researchers in the past hundreds of years of genetics have been taught to believe what population geneticists decided to believe. However, the population geneticists never learned about the basic principles of biology or the levels of biological organization required to link the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man.

With no understanding of biology, and no experimental evidence to support their theories, population geneticists have since simply decided that mutation-initiated natural selection must be reduced to mutation-driven evolution. What choice do they have? No one ever showed what was naturally selected, or how genes were fixed in the populations of organisms that evolved. Now, they must believe that mutation-driven evolution “just happens.” It must, because statistical analyses say it happens … somehow.

Nothing else matters to a theorist but the math, as we’ve recently seen, especially when researchers wrote in 2011: “…we will not consider geographical and ecological factors because of space limitation. Our primary purpose is to clarify the roles of mutation and selection in the evolution of reproductive isolation…“    Anyone who is familiar with how Darwin’s theory was repeatedly inseminated with ideas from population genetics will recognize how fertilizing the minds of theorists led to the bastardization of Darwin’s theory and its bastard child: Mutation-Driven Evolution. All that is left of mutation-initiated natural selection is a theory of how constraint-breaking mutations somehow cause it.

Meanwhile, serious scientists have learned that The perceptual logic of smell links the nutrient-dependent pheromone-controlled de novo creation of olfactory receptor genes from their presence in unicellular spermatazoa to our experience-dependent receptor-mediated sense of smell via the conserved molecular mechanisms that link ecological variation to ecological adaptations in species from microbes to man. But don’t try to tell a theorist about biologically based cause and effect. They didn’t want to hear about detailed mechanisms before, and it’s too late now for them to learn about the requirement for experimental evidence. That requirement makes them look like fools who thought that the ecological, social, neurogenic, and socio-cognitive niche construction manifested in increasing organismal complexity “just happened.”

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Combating evolution with facts about ecological adaptations

March 7, 2014 | James Kohl

Science 7 March 2014: Vol. 343 no. 6175 pp. 1088-1089. DOI: 10.1126/science.1247472 PERSPECTIVE: MEDICINE

Combating Evolution to Fight Disease

  1. Christine Queitsch

Excerpt: “Molecular biology and evolutionary biology have been separate disciplines and scientific cultures: The former is mechanistic and focused on molecules; the latter is theoretical and focused on populations. However, these domains are beginning to converge in laboratories addressing molecular mechanisms that explain how evolutionary processes work…”

My comment: Darwin probably anticipated the insemination of population genetics that led to the bastardization of his detailed observations in the “Modern Synthesis.” He politely insisted that ‘conditions of life’ be considered before natural selection.

Darwin could not have known that what is now known about conserved molecular mechanisms, which link the epigenetic landscape to the physical landscape of DNA in the organized genomes of microbes to man, would reveal the biological fact that life is nutrient-dependent. Therefore, Darwin must have based the entirety of works on at least one assumption about his ‘conditions of life.’ He correctly assumed that life is nutrient-dependent.

However, there are two ‘conditions of life.’ Not even Darwin could have anticipated that what has since become known would reveal the biological fact that the physiology of reproduction is controlled by the metabolism of nutrients to species-specific pheromones. Therefore, until publication of “Pheromones: a new term for a class of biologically active substances” in 1959, everything else added to Darwin’s astute observation-based claims was added on faith.

Evolutionary theorists convinced biologists to believe that mutation-initiated natural selection was possible, which meant that sexual selection must also somehow result from mutations. Simply put, there was no other acceptable explanation! Anyone who objected to being called a mutant was silenced.

Biologists who somehow knew, like Darwin, that mutation-driven evolution was not possible, were not accepted among members of the academic priesthood who became the gatekeepers of scientific information. It is not scientific information, until the academic priesthood tells us it is, and  they claimed that evolutionary theory was based on scientific information.

Anyone who claimed that mutation-driven evolution was a “just a theory” was considered to be just another ‘crank’ or worse — a creationist. Few people realize that Dobzhansky was a creationist who demanded that theories be tested and supported by experimental evidence.

Rosenberg and Queitsch now note the published work that contains Dobzhansky’s rarely acknowledged claim:  ”I am a creationist and an evolutionist. Evolution is God’s, or Nature’s, method of Creation.” They also declare the need for “Deep understanding of the mechanisms that generate variation at the molecular level…” Deep understanding does not come from theory.

In 1964, Dobzhansky had something to say about that, too. “The notion has gained some currency that 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!”

Others complain when I take that quote out of context. I do it anyway because I like to emphasize the difference between epigenetic effects and behavioral affects. Those who complain are usually atheistic theorists and/or biology teachers who have arrogantly ignored Dobzhansky’s creationist beliefs about effects on genes, which must somehow be linked to affects on behavior. Occasionally, even medical professionals claim to know things that are not biologically plausible.

Problems with the “modern synthesis” now lead us back to the facts about biologically based cause and effect that Darwin and Dobzhansky approached with humility. These are the same biological facts that evolutionists approached with ignorance about behavioral affects and the arrogance that accompanies that ignorance.  Rosenberg and Queitsch echo the sentiments of those who have been subjected to academic suppression.

Clearly, however, “nothing in evolution makes sense except in the light of biology” is not an exaggeration. It is a common sense statement about the biologically plausible genesis of functional cell types. Population genetics and evolutionary theories abandoned the biophysical constraints of ecological variation, networks of  glycosylation,  and the physiology of reproduction, which enable epigenetically-effected nutrient-dependent pheromone-controlled receptor-mediated ecological adaptations and species diversity via the complexities of protein folding and niche construction.

Most of us have been left to discuss aspects of evolution when we could have been discussing the molecular epigenetics of ecological adaptations, which biophysically constrain the constraint-breaking mutations that theorists claim cause species diversity and also pathology. Is there a model for that evolutionary duality?

If there is no model of evolutionary duality that is supported by experimental evidence, it’s time for biophysicists to tell theorists and pathologists how to differentiate between theories about the genesis of different cell types and the biological facts about the nutrient-dependent pheromone-controlled ecological adaptations that enable the genesis of different cell types in individuals of different species. Simply put, it’s time to stop trying to explain ecological adaptations in the context of mutations and evolution.

————————————————————

I edited the above comment to Science magazine on this article, and the comment I submitted on 3/7/14 was approved and posted on 3/10/14

“Darwin probably anticipated the insemination of population genetics that led to the bastardization of his detailed observations in the “Modern Synthesis.” He politely insisted that ‘conditions of life’ be considered before natural selection.

There are two ‘conditions of life.’ It is nutrient-dependent and pheromone-controlled. Rosenberg and Queitsch now note the work with Dobzhansky’s rarely acknowledged claim: “I am a creationist and an evolutionist.” They also declare the need for “Deep understanding of the mechanisms that generate variation at the molecular level…”

Deep understanding of the ‘conditions of life’ does not come from theory.

Problems with the “modern synthesis” now lead us back to the facts about biologically-based cause and effect that Darwin and Dobzhansky approached with humility, which are the same biological facts that evolutionists approached with ignorance about behavioral affects and the arrogance that accompanies that ignorance. Rosenberg and Queitsch echo the sentiments of those who have been subjected to academic suppression.

Clearly, however, “nothing in evolution makes sense except in the light of biology” is not an exaggeration. It is a common sense statement about the biologically plausible genesis of functional cell types. Population genetics and evolutionary theories abandoned the biophysical constraints of ecological variation and the physiology of reproduction, which enable epigenetically-effected nutrient-dependent pheromone-controlled receptor-mediated ecological adaptations and species diversity via the complexities of protein folding and niche construction.

It’s time for biophysicists to tell theorists and pathologists how to differentiate between theories about the genesis of different cell types and the biological facts about the nutrient-dependent pheromone-controlled ecological adaptations that enable the genesis of different cell types in individuals of different species. Simply put, it’s time to stop trying to explain ecological adaptations in the context of mutations and evolution. “

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Explanatory duality: Science in flies is not Nature in butterflies

March 6, 2014 | James Kohl

Science 7 March 2014: Vol. 343 no. 6175 p. 1055 DOI: 10.1126/science.343.6175.1055-f

  • This Week in Science

Evolutionary Duality

When ecological divergence involves traits that also contribute to mating behavior, such divergence could lead to rapid reproductive isolation and speciation. However, there are very few experimental demonstrations of such “dual” traits. Chung et al. (p. 1148, published online 13 February) now demonstrate that specific cuticular hydrocarbons are a dual trait that affects both desiccation resistance and mate choice in the widely distributed Australian species Drosophila serrata. These compounds have largely been lost from its rainforest-restricted, desiccation-sensitive, closely related sibling D. birchii.

My comment: Fatty acid metabolism and pheromone production link a single gene to ecological adaptations and species diversity in flies.

My comment to Science magazine was submitted on 3/7/14 and approved and posted on 3/10/14

Ecological variation and adaptations associated with a single gene and with nutrient-dependent pheromone-controlled mate choice in flies became meaningful mutations in the regulatory sequences of a single gene in butterflies associated with mimicry.

Evolutionary biology: Sex, lies and butterflies

Has anyone seen experimental evidence that suggests that the molecular mechanisms that enable species diversity are different in flies and butterflies?

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