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Monogenic ecological divergence is pheromone-controlled

Posted on February 14, 2014 by James Kohl.

A Single Gene Affects Both Ecological Divergence and Mate Choice in Drosophila

Excerpt: “…the direct contribution of ecological divergence to speciation is uncertain, in part because relatively few systems have been investigated experimentally, and the genes affecting dual traits have not been identified.”

My comment to Science Magazine (submitted Fri Feb 14, 2014 at 4:06 AM; published Tuesday, Feb 18, 2014 at 12:28 pm)

“In flies, ecological and social niche construction can be linked to molecular-level cause and effect at the cellular and organismal levels via nutrient-dependent changes in mitochondrial tRNA and a nuclear-encoded tRNA synthetase. The enzyme enables attachment of an appropriate amino acid, which facilitates the reaction required for efficient and accurate protein synthesis (Meiklejohn et al., 2013).” — Kohl (2013) Nutrient-dependent pheromone-controlled adaptive evolution: a model.

Chung et al (2014) extend the concept of nutrient-dependent pheromone-controlled epigenetically-effected alternative splicings of pre-mRNA from our section on molecular epigenetics in a 1996 Hormones and Behavior review article. Elekonich and Robinson (2000) already did that for insects before Elekonich and Roberts (2005) used the conserved molecular mechanisms approach in an extension to “Honey bees as a model for understanding mechanisms of life history transitions.”

Someone else may help others to understand the experimental evidence from this study in the context of mutation-initiated natural selection, if it does not fully support the paradigm shift to a model of ecological variation, natural selection for food, and metabolism of nutrients to species-specific pheromones that control the physiology of reproduction.

However, in the context of ecological adaptations I think this experimental evidence establishes the fact that “Olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans.” Kohl (2012) 

———————————————————–

Addendum:

For comparison of cause and effect in the current report co-authored by Sean B. Carroll to his historical representations see:

— and Carroll, S.B. (2008) The regulation and evolution of a genetic switch controlling sexually dimorphic traits in Drosophila. 

Excerpt: “The properties of these CREs resolve the question of how the effects of mutations can be restricted to one sex.”

My summary: One of the two sexes must have mutated into existence.

For a comparison to my historical perspective on ecological adaptations, which was co-authored by a researcher with my surname, see also:

Kohl, Johannes. et al. (2013) A Bidirectional Circuit Switch Reroutes Pheromone Signals in Male and Female Brains.

Excerpt 1):  …


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The evolutionary process is ecological adaptation

Posted on February 14, 2014 by James Kohl.

I posted a few hours ago because Sean B. Carroll’s comments in Scientific American: Is America Evolving on Evolution? seemed to directly conflict with what is currently being touted by Masatoshi Nei, author of Mutation-Driven Evolution.

Nei says that natural selection isn’t the driving force of evolution. Carroll inferred that it is. He wrote: “In the evolutionary process a trait expands through a population when individuals possessing it survive longer and reproduce more than do those lacking the trait.”  Isn’t that evolutionary process called natural selection?

Isn’t natural selection the evolutionary process that Nei says is not the driving force of evolution? Haven’t Nei and Carroll both been claiming that mutations somehow cause evolution as they might if there was such a thing as mutation-initiated natural selection, which there may or may not be? Is anyone else confused when one proponent of mutation-driven evolution eliminates natural selection as the driving force of evolution at the same time another proponent of mutation-driven evolution relies on natural selection to drive the evolutionary process?

If so, it gets worse. Nei and Nozawa (2011) decided to not consider ecological factors in their attempt to clarify the roles of mutation and selection. As senior author, Carroll now writes:

1) “…changes in CHC production in ecologically-diverging populations may be an important general contributor to insect speciation.”

CHC production is nutrient-dependent and CHCs

2 “…act as pheromones which influence mate choice and mating success.”  See for quotes 1 and 2: “A Single Gene Affects Both Ecological Divergence and Mate Choice in Drosophila.”

Anyone who thought a consensus had ever been reached about cause and effect in the context of mutation-initiated natural selection, has now seen natural selection extracted. Nei and others  say it is no longer the driving force of mutation-driven evolution. Nei has also previously excluded consideration of ecological factors from mutation-initiated evolution.

Carroll seems to think that natural selection is important to evolution but he just inferred that ecological variation is an important general contributor to pheromone-controlled insect speciation and did not mention mutations in the context of ecological variation.

I think I can help Nei and Carroll ‘come to terms’ with the basic principles of biology and levels of biological organization required to link ecological variation to speciation in species from microbes to man. The terms they need to come to use are used in my model of nutrient-dependent pheromone-controlled ecological …


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The evolutionary process isn’t a process

Posted on February 13, 2014 by James Kohl.

Scientific American invites essays from experts on topical issues in science and technology for their SA Forum. Here’s what their expert, Sean B. Carroll thinks is positive news about Americans’ views on evolution. Is America Evolving on Evolution?

Article excerpt 1) : “Three-and-a-half billion years of life’s history has taught us one inescapable truth: as the Earth changes, life changes along with it.”

Article excerpt 2) : “In the evolutionary process a trait expands through a population when individuals possessing it survive longer and reproduce more than do those lacking the trait.”

My comment: Although many people were taught that the history of life extends across three-and-a-half billion years, others have learned that ecological variation requires life to rapidly adapt via ecological, social, neurogenic and socio-cognitive niche construction. There is experimental evidence of niche construction, and we see rapid ecological adaptation everywhere we look, especially if it is viewed in the context of  the nutrient-dependent pheromone-controlled physiology of reproduction. Simply put, what we see is that Darwin’s ‘conditions of life’ lead to increasing organismal complexity in species from microbe to man.

One of Darwin’s ‘conditions of life’ is that organisms must find food. Another of his ‘conditions of life’ is that organisms must reproduce. If we look at increasing organismal complexity from the perspective of evolution via acquisition of food and its epigenetic effects on genetically predisposed reproduction, we see what population genetics has taught us about biology, which is that mutation-driven evolution “just happens.”

Until recently, most students were taught that mutation-initiated natural selection caused evolution. Now, even Masatoshi Nei, author of “Mutation-Driven Evolution,” claims that “Mutation, Not Natural Selection, Drives Evolution.” In an interview for Discover Magazine, he reveals other things about evolution that Sean B. Carroll and other experts don’t seem to know.

For example, “Molecular evolutionary biologist Masatoshi Nei says Darwin never proved natural selection is the driving force of evolution — because it isn’t.” Sean B. Carroll tells us: “In the evolutionary process, a trait expands through a population when individuals possessing it survive longer and reproduce more than do those lacking the trait.” Nei tells us Carroll is wrong, and Nei has been telling others they are wrong since 1987.

Darwin told us that variation must be involved in species diversity, which became obvious when people looked at the diversity. Others decided that the diversity must be due to mutation-initiated …


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Do vertebrate wide mutations cause a human monogenic disorder?

Posted on February 12, 2014 by James Kohl.

In the context of vertebrate wide mutations, mutation-driven evolution is extended across species in this research journal article and in this report about it:

Single nucleotide polymorphism in the neuroplastin locus associates with cortical thickness and intellectual ability in adolescents

Journal article excerpt: “NPTN and other genes involved in neurite outgrowth have recently been identified as direct targets of FOXP2, a transcription factor that when mutated causes a monogenic speech and language disorder in humans and the reduced dosage of which impairs synaptic plasticity, motor-skill learning and ultrasonic vocalizations in mice, and disrupts vocal learning in songbirds. In agreement with our data, this suggests that similar to FOXP2, NPTN may be involved in learning vocal and nonvocal skills. Furthermore, functional polymorphisms in the NPTN promoter that may confer susceptibility to schizophrenia have been identified.”

My comment: Natural selection is removed from consideration in a forthcoming Discover magazine interview article about the author of the book and concept of Mutation-Driven Evolution.

Two questions remain unanswered:

1) What causes mutations that cause monogenic disorders.

2) How does mutation-driven evolution occur without natural selection?

Now that researchers have extended the concept of mutation-driven evolution across species and tentatively linked specific mutations to a monogenic human disorder of development, they must also ready themselves for questions like this:  How are vertebrate-wide mutations that alter similar traits such as ultrasonic vocalizations, singing in birds, and human language development transferred from one species to another with or without the involvement of natural selection?

See also:

1) Mutant enzymes challenge all assumptions: “Mutant proteins… never have been activated in the first place, and residues that we presumed were important actually play roles quite unlike what we anticipated.”

2) Ecology in the genomics era of a degraded planet: “Our planet’s biological legacy—including all the different habitats on Earth and all the different species that live in them—is the result of eons of natural selection.”

For comparison to the what appears to be collectively unequivocal and repeated refutations of mutation-initiated natural selection in the context of mutation-driven evolution, see:

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) …


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Natural selection is not the driving force of evolution

Posted on February 11, 2014 by James Kohl.

Discover Magazine Table of Contents March 2014

DISCOVER Q&A

Mutation, Not Natural Selection, Drives Evolution  

by Gemma Tarlach

Molecular evolutionary biologist Masatoshi Nei says Darwin never proved natural selection is the driving force of evolution — because it isn’t.

Excerpt: “…it’s his natural selection-busting theory, which Nei developed in the ’80s and expanded on in the 2013 book Mutation-Driven Evolution, that the researcher wants to see embraced, cited and taught in schools.

My comment: Ecological variations cause epigenetically effected adaptations sans mutations. I would like to to see that biological fact embraced, cited and taught in schools.

The reason I would like that biological fact embraced is because I’m tired of comments about my model from uninformed people who think they are experts.

For example, in July 2013, I wrote: “… this statement and any statement or inference like it is WRONG: Random mutations are the substrates upon which directional natural selection acts.”

Jay R. Feierman (responded): I am absolutely certain that if you showed this statement to any professor of biology or genetics in any accredited university anywhere in the world that 100% of them would say that “Random mutations are the substrate upon which directional natural selection acts” is a correct and true statement.

Feierman’s antagonism has been unrelenting: I also wrote:

James Kohl: Natural selection

“If you have variation, differential reproduction, and heredity, you will have evolution by natural selection as an outcome. It is as simple as that.”

The variation is nutrient availability and nutrients metabolize to species-specific pheromones that control reproduction and heredity. Evolution by natural selection cannot be the outcome if something is not first selected. Selection is always for nutrients. It is as simple as that.

If it is not that simple, someone needs to explain why they believe in a theory of mutation-driven evolution and detail how mutation-driven evolution occurs.

Jay R. Feierman: It is very sad for me to see that when several different people on this group, all with doctorate degrees, tell you that you are not correct, you don’t consider that they might be telling you something helpful. Instead, you respond with arrogance and ignorance. I’ll add my voice to the other people on this group who have told you that you are not correct in terms of your understanding of what “variation” means in …


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What is the vomeronasal organ (VNO)?

The vomeronasal organ (VNO) is a cone-shaped organ in the nasal cavity, which is believed to be one of the body's receptors of pheromones. More, specifically, the VNO, which is part of the accessory olfactory system in the nose, does not respond to normal scents, but may detect odorless, barely perceptible pheromones.

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Learn more about the science behind pheromones here.

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