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Nutrient dependent pheromone controlled morphogenesis

Posted on April 29, 2013 by James Kohl.

Pheromone-Induced Morphogenesis Improves Osmoadaptation Capacity by Activating the HOG MAPK Pathway

Excerpt: “We report here that pheromone stimulation of osmoadapted cells leads to a steady state with higher glycerol turnover. Such cells are able to adjust faster to changes in external osmolarity: Faced with a new osmotic shock, pheromone-treated cells recovered twice as fast than untreated cells. Such an advantage may justify the energy invested in seemingly futile cycles of synthesis and degradation or loss.”

Arthropods and inherited bacteria: from counting the symbionts to understanding how symbionts count

Excerpts: “…symbionts mediate variation in heat tolerance, plant use and body color [5,9]. For instance, the symbiont Rickettsiella changes the body color of the aphid host from red to green, and is thus likely to influence relative susceptibility to predators [9].”

“The… source of adaptation – a symbiont in other members of the ecological community rather than a mutation of existing genetic material – is likely to change our understanding of arthropod evolution.”

Feeding plasticity in the nematode Pristionchus pacificus is influenced by sex and social context and is linked to developmental speed

Excerpt: “Given form-specific feeding differences, the sexual differences in the mouth dimorphism in a population could affect the partitioning of resources among conspecifics, possibly leading to an ecological selection for the sexual dimorphism (Shine 1989). ”

Evolution of mir-92a Underlies Natural Morphological Variation in Drosophila melanogaster

Excerpt: “We report here the first example of natural variation in the expression of a miRNA causing morphological change.”

My comment: An aging 60-ish college student unfamiliar with the basic principles of biology and levels of biological organization wrote: ” That a mutation in a miRNA (a molecule expressed as a part of the normal, evolved regulatory process), in this case mir-92a (Drosophila), results in a morphological difference is not surprising.”

The authors of the article on Drosophila do not mention mutational cause, and their emphasis on “Natural Morphological Variation” is quite clear.

The news release states: “By overexpressing the gene in the legs of the fruit flies, the scientists were able to cause hair loss on the animals’ legs.” They used a heat shock technique during larval development to induce a “Natural Morphological Variation”. The journal article states: “…we overexpressed UAS-mir-92a [16] using a heatshock-GAL4 driver in pupal legs between 8 and 24 hr after puparium formation (APF), when the naked valley pattern is determined [6].”

In my model, any additional heat alters the typical nutrient-dependent microRNA / messenger RNA balance-controlled thermodynamics of intracellular signaling, chromatin remodeling, protein biosynthesis, stochastic gene expression, and organism-level thermoregulation. Those alterations lead to  changes associated with metabolism of nutrients to species-specific pheromones and to the morphological changes associated with species diversity.

For contrast to the mutations-theory approach, this “…diversity becomes, however, reasonable and understandable if the Creator has created the living world not by caprice but by evolution propelled by natural selection… Evolution is God’s, or Nature’s, method of Creation.” Most of us also know that “Reproductive isolation evidently can arise [via Natural Selection for nutrients] with little or no morphological differentiation.”

The model organism I use is the honeybee, since changes in the morphology of the worker bees’ brain are clearly nutrient-dependent and pheromone-controlled. Thus, the Creation of diversity does not arise via mutations that alter morphology, but by the epigenetic effects of nutrients and pheromones on the thermodynamics of intracellular signaling and intranuclear interactions. Those interactions result in de novo protein biosynthesis required for finely-tuned organism-level thermoregulation of immune system function, reproduction, species divergence, and balanced selection, which results in epistasis.

Only by introducing mutations theory can others continue to deny the overwhelming evidence for nutrient-dependent pheromone-controlled adaptive evolution via epigenetic effects on the microRNA / messenger RNA balance. Be sure to watch for insertion of that ridiculous theory again, even in comments on articles that clearly demonstrate cause and effect sans mutations.

Introducing mutations theory misrepresents the works of others, like Dobzhansky, Francis Collins (The Language of God), and me (Nutrient-dependent / Pheromone-controlled thermodynamics and thermoregulation). But, for some reason, there are many people who still do not realize that any mutations theory of adaptive evolution has no basis in biological fact. Instead, mutations theory can eve retard scientific progress in the context of cardiovascular risk.

Intestinal Microbial Metabolism of Phosphatidylcholine and Cardiovascular Risk

Just as the bacteria arthropods and nematodes eat changes their morphology and pheromone production sans mutations, the gut bacteria we nutritionally support contributes to the production of species-specific pheromones that will someday be used to assess cardiovascular risk via a non-invasive breath test. See, for example:  Noninvasive measurement of plasma triglycerides and free fatty acids from exhaled breath.

But first, others must help stop the mutational-cause nonsense that continues to be propagated by under-informed theorists.

 

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James Kohl
Retired medical laboratory scientist

James Kohl




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