Experimental evidence and examples vs opinions

February 22, 2014 | James Kohl

The Age of Olfactory Bulb Neurons in Humans (2012, senior author Frisén)

Abstract excerpt: Results show that olfactory bulb neurons in humans are as old as the individual and argue that adult olfactory bulb neurogenesis is minimal in humans.

Journal article conclusion: “Functional studies in rodents have implicated adult neurogenesis in olfactory memory formation, odorant discrimination, and social interactions (Lazarini and Lledo, 2011). The lack of comparable adult olfactory bulb neurogenesis in humans poses the question whether these functions are mediated by conceptually different mechanisms in humans, or whether the more limited dependence on olfaction in humans compared to rodents in part may be due to the lack of one type of plasticity, adult neurogenesis.”

Reported as: No new neurons in the human olfactory bulb

Excerpt: “This is a strong indication that there is no significant generation of new neurons in this part of the brain, something that sets humans apart from all other mammals.”

My comment: Experimental evidence clearly shows that conserved molecular mechanisms link the epigenetic landscape to the physical landscape of DNA in the organized genome of species from microbes to man via olfactory memory formation, odorant discrimination, and social interactions. Food odors and social odors  link ecological variation from the impact of olfactory/pheromonal input in rats to the differentiation of our cell types and to our morphological and behavioral phenotypes. The importance of acknowledging the conserved molecular mechanisms is apparent in the following article about:

Lifelong Neuronal Rebirth

By Kate Yandell | February 20, 2014

Excerpt: Eventually, Frisén and his colleagues’ findings could impact regenerative medicine research and the treatment of neurodegenerative diseases.

My comment: In less that two years, Frisén and his colleagues’ findings have gone from denying the similarities across species of mammals, to exemplifying them.  What appears to have not changed is Frisén’s opinion about the importance of the sense of smell in rats compared to its importance in humans.

2012 “Humans are less dependent on their sense of smell for their survival than many other animals, which may be related to the loss of new cell generation in the olfactory bulb…” says Professor Frisén.

2014 “It is clear that we are much less dependent on olfaction—and have a less developed sense of smell—than most other mammals,” Frisén explained in an e-mail to The Scientist.

My [edited] comment to the Scientist:

The perceptual logic of smell “…growing recent evidence for expression of olfactory receptors in non-chemosensory tissue” implies that “..the complexity of the olfactory genome may hold secrets for more than understanding olfaction alone.”

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.

Pheromones and the luteinizing hormone for inducing proliferation of neural stem cells and neurogenesis links my “atoms to ecosystems” approach from food odors and pheromones to neurogenic niche construction, neurodegenerative diseases and to morphological and behavioral phenotypes in species from roundworms to humans.

For example, see: System-wide Rewiring Underlies Behavioral Differences in Predatory and Bacterial-Feeding Nematodes “We uncover a massive rewiring in a complex system of identified neurons, all of which are homologous based on neurite anatomy and cell body position.”

No experimental evidence suggests that “…we are much less dependent on olfaction—and have a less developed sense of smell—than most other mammals….” That is an ecologically invalidated opinion, which Professor Frisén’s work helps to expose in the context of neurogenic niche construction.

It is also an opinion that is biologically implausible. Like other opinions about cause and effect, it must be placed into the context of the ecological adaptations that enable neurogenic niche construction. Clearly, we cannot be any less dependent on olfaction for nutrient acquisition or the nutrient-dependent pheromone-controlled physiology of our reproduction than any other organism with conserved molecular mechanisms. And those mechanisms link the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man. The organized genomes in roundworms are organized by the molecular mechanisms that enable neurogenic niche construction in humans.

In that context, opinions about the relative salience of different types of sensory input, which epigenetically effect the molecular mechanisms that affect behavior, and opinions about the primacy of our sense of smell defy The perceptual logic of smell. Ernst et al., tells us it is time for our opinions to become acquainted with biological facts about ecological, social, neurogenic, and socio-cognitive niche construction.

Addendum: Even when it is Frisén who reports results that imply he previously misrepresented biological facts, his opinion about the importance of the human sense of smell compared to its importance in other mammals has not changed. The question arises: why waste time on experiments that provide evidence if the experimental evidence does nothing to change your opinions about the conserved molecular mechanisms of biologically-based cause and effect? However, perhaps the science journalist do not know how to ask scientists the right questions, which would enable accurate reporting of their results.

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Ecological speciation: No alternative

February 21, 2014 | James Kohl

Evidence for Ecological Speciation and Its Alternative

Excerpt: “… the discovery that reproductive isolation can be brought about by ecological adaptation in ordinary phenotypic traits bridges Darwin’s science of speciation and our own.

“The most obvious shortcoming of our current understanding of speciation is that the threads connecting genes and selection are still few. We have many cases of ecological selection generating reproductive isolation with little knowledge of the genetic changes that allow it.”

My comment: Experimental evidence of cause and effect supports scientific progress. I used experimental evidence of conserved molecular mechanisms that are obviously responsible for ecological adaptations in the context of nutrient-dependent pheromone-controlled adaptive evolution: a model.  I regret the implication that adaptive evolution occurred, but reviews that are not framed in the context of evolution are not well-received. Simply put, researchers must mislead others an make them think their opinions of cause and effect might be validated, or they may not read the latest published works on ecological adaptations, which means the work will not receive critical evaluation.

One critical evaluation of my model was reported in a book in 2011:  ‘This model is attractive in that it solves the “binding problem” of sexual attraction. By that I mean the problem of why all the different features of men or women (visual appearance and feel of face, body, and genitals; voice quality, smell; personality and behavior, etc.) attract people as a more or less coherent package representing one sex, rather than as an arbitrary collage of male and female characteristics. If all these characteristics come to be attractive because they were experienced in association with a male- or female-specific pheromone, then they will naturally go together even in the absence of complex genetically coded instructions.”  (p. 210)

Since then, experimental evidence to support the model, which solved the “binding problem” of sexual attraction, has continued to accumulate. No experimental evidence supports the idea of mutation-driven evolution of sexual attraction has been published. Instead, Evidence for Mito-Nuclear and Sex-Linked Reproductive Barriers between the Hybrid Italian Sparrow and Its Parent Species portrays ecological adaptations.

Excerpt:  “…the fact that HSDL2‘s protein product is located within mitochondria [37], [44] supports its candidacy as an RI gene. HSDL2 is thought to be involved in fatty acid metabolism, although its exact functions are unknown [44].”

My comment:  In my model this fact links the nutrient-dependent protein product to the metabolism of fatty acids to species-specific pheromones that control reproduction. The claim that the exact functions of  HSDL2 are unknown are akin to claims that no one knows exactly which fatty acid metabolites might effect the mixture of nutrient-dependent metabolites that act as species-specific pheromone signatures. Despite the model that links nutrient uptake to pheromone production and species diversity, the portrayal of ecological adaptations in this study will probably be critically reviewed as if  it exemplified mutation-driven evolution via natural selection for whatever was selected. Only if reviewers dig deep enough into the confusion of the text will they find that one species appears to have been selected for mito-nuclear interactions and loci on the Z chromosome. That links the metabolism of nutrients to species-specific pheromones and chromosomal rearrangements, which places the molecular mechanisms of speciation into the context of biophysical constraints on beneficial mutations. Instead of beneficial mutations, which are not known to occur, nutrient-dependent pheromone-controlled reproduction seems likely to have contributed to de novo gene creation and chromosomal rearrangements that link common molecular mechanisms to species diversity in species from microbes to man.

For comparison, Estrogen receptor α polymorphism in a species with alternative behavioral phenotypes and also with different morphological phenotypes  clearly exemplifies nutrient-dependent pheromone-controlled ecological adaptations. The ecological adaptations obviously arise from epigenetic effects of the sensory environment. The adaptations are associated with differences in parental feeding that result in chromosomal rearrangements and in transgenerational epigenetic inheritance of morphological and behavioral phenotypes without reproductive isolation that might lead to speciation.

Everything about the conserved molecular mechanisms that might lead to species diversity goes together in the absence of complex genetically coded instructions in Estrogen receptor α polymorphism in a species with alternative behavioral phenotypes. Nothing that is known about the conserved molecular mechanisms of ecological adaptations fits into the context of Evidence for Mito-Nuclear and Sex-Linked Reproductive Barriers between the Hybrid Italian Sparrow and Its Parent Species. The evidence may initially appear to exemplify mutation-driven evolution, which means a critical evaluation of experimental evidence may already be overdue.

Mutation-driven evolution makes no attempt to solved the “binding problem” of sexual attraction. Thus, the theory does not seem to fit very well into the experimental Evidence for Mito-Nuclear and Sex-Linked Reproductive Barriers. The question arises,  how is the physical evidence of nutrient-dependent mito-nuclear interactions linked via mutations to reproductive barriers?  The answer to the question can be placed into the context of experimental evidence that links epigenetically-effected Estrogen receptor α polymorphism to alternative morphological and behavioral phenotypes. Experimental evidence that links epigenetically-effected morphology and behavior to species diversity via conserved molecular mechanisms could then be critically reviewed for comparison to explanations of how mutation-driven evolution might somehow result in species diversity.

I suggest that Evidence for Mito-Nuclear and Sex-Linked Reproductive Barriers and Estrogen receptor α polymorphism, which is linked to alternative morphological and behavioral phenotypes, be compared in the context of nutrient-dependent pheromone-controlled de novo creation of olfactory receptor genes. This might lead to an explanation of how mutations appear to result only in the loss of genes accompanied by the creation of pseudogenes. The pseudogenes do not perturb protein folding like mutations do, so the pseudogenes are not eliminated from the DNA of the organized genome like they would be if they were mutated genes that perturbed protein folding. If anything, the pseudogenes appear instead to be placed on hold in case their reactivation and unfolding might be required if the epigenetic effects of food odors and controlled expression of genes by pheromones was ever required for species diversification in an unpredictable environment of ecological variation. There’s a model for that!

Looking for the bird Kiss: evolutionary scenario in sauropsids

Excerpt: The loss of Kiss function in birds may also reflect the plasticity in the neuromediators and their receptors involved in the control of GnRH neurons and reproductive function throughout vertebrate evolution.”

My comment: In my model, stabilization of the genome occurs via the conserved molecular mechanisms of nutrient-dependent pheromone-controlled ecological adaptation and the chromosomal rearrangements that may or may not result in species diversity via substitution of the achiral amino acid glycine in the GnRH peptide that appears to be conserved in the vertebrate genome across 400 million years ecological adaptations. An established biological core of vertebrate reproduction enables rapid diversification of species that fill ecological niches. The ecological niches link differences in the amniote lineage to differences in the sauropsid lineage and the mammalian lineage via nutrient-dependent pheromone-controlled amino acid substitutions that differentiate the cell types of all genera.

The link from olfactory/pheromonal input to nutrient-dependent pheromone-controlled amino acid substitutions and the de novo creation of olfactory receptor genes and to nutrient-dependent pheromone-controlled variations in GnRH pulse frequency establishes the ligand-receptor link between GnRH and its receptor. The ligand-receptor link is the biological basis of my explanations for how the epigenetic landscape becomes the physical landscape of DNA in the organized genomes of species as diverse as egg-laying dinosaurs and birds. Conserved molecular mechanisms of nutrient-dependent pheromone-controlled species-specific reproduction establish how everything known about ecological adaptations in the context of the ecological variations may result in speciation in species from microbes to man.

The alternative to examination of genes and pseudogenes in different lineages is to continue to evoke the idea of “constraint-breaking” mutations in genes that somehow might be responsible for mutation-driven evolution. The biophysical constraints that lead to mammals from amniotes such as dinosaurs and birds can be removed from consideration via suggestion. That suggestion allows some people to continue believing in that mutations led to difference in birds and mammals. Therefore, they can continue to believe that mutation-driven evolution occurs outside the context of biophysical constraints in all genera. However, with beliefs like that, there is no reason to  teach students about physics, chemistry, or biology. They need only be taught to believe in Masatoshi Nei’s “constraint-breaking mutations” that he thinks enable Mutation-Driven Evolution.

…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.

I’m reminded of the song: “Do you believe in magic?” Obviously many people do, but I don’t think that the “magic” of mutation-driven evolution should be taught to students. There’s no model for that. It’s just Nei’s suggestion of what should be taught.

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Preventing analytical thinking

February 20, 2014 | James Kohl

Reliance on social groups for answers pre-empts motivation for independent analytical thinking.

February 19th, 2014.

Excerpt: “The social information is useful-it helped participants get to the answer-but it didn’t help them understand the thinking process underlying that answer,” Shariff said. “So when confronted with another similar question, it’s as if they had learned nothing about how to solve it.”

My comment: What’s reported in this article is exemplified among participants in the ISHE’s yahoo group and in many other forums for discussion. For example, it seems likely that Feierman edits my posts to ensure that the social structure of the group does not vary from how it has historically been maintained.

The problem in most discussions is that participants collectively attack anyone with ideas based on independent thinking, so that they can potentially oust an outsider who might otherwise force them to begin thinking analytically. By editing my responses to their attacks, and blocking some — but not all other — contributions, Feierman prevents participants from seeing how new data from experiments collectively supports ecological adaptation and refutes untested ideas about how natural selection might occur — if it occurred for anything other than food, as is required to meet one of Darwin’s ‘conditions of life’. For example, natural selection cannot possibly select for Pedophilia in any context, including what is represented in Feierman’s (2011) book.

As some participants now know, however, preventing others from participating in discussions of how scientific progress is made via experimental evidence, ultimately fails. Other social groups learn about what is currently known from sources that do not limit dissemination and discussion of accurate information.

For example, if Feierman were not editing and blocking some of my posts, others would already be discussing recent results that establish the fact that 1) The life cycle of Drosophila orphan genes and 2) Looking for the bird Kiss: evolutionary scenario in sauropsids and 3) Embryonic Cerebrospinal Fluid Nanovesicles Carry Evolutionarily Conserved Molecules and Promote Neural Stem Cell Amplification fully support a model of ecological adaptations that refutes the theory of mutation-driven evolution.

Summaries:

1) provides a missing link that helps others to understand orphan gene dynamics in the context of nutrient-dependent pheromone-controlled ecological adaptations.

2) links nutrient-dependent pheromone-controlled ecological adaptations from dinosaurs to birds via the conserved molecular mechanisms of alternative splicings and chromosomal rearrangements.

3) links nutrient uptake to the microRNA/messenger RNA balance and to differences in the embryonic development of rat and human brains.

The media reports on these articles do not facilitate the full understanding of what they show when considered in the context of what was or will be reported within in few days.

1) Newly created genes frequently lost, driving evolution: Mystery solved by recent research

2) My synopsis of what will be reported: Conserved molecular mechanisms link nutrient-dependent hormone-organized and hormone-activated behavior to ecological adaptations via gonadotropin releasing hormone.

3) Tiny ‘garbage collectors’ help control brain development (see also: New mechanism that permits selective capture of microRNAs in nanovesicles that shuttle between cells) report on how microRNAs, which are small RNA molecules, regulate the expression of specific genes.

The specific genes include the evolutionarily conserved FOXP2 gene, which appears to be conserved in the context of two microRNAs that link social singing in songbirds to human language development.

Participants who rely on social groups for answers to questions about biologically-based cause and effect will almost undoubtedly continue their discussions of theory and avoid discussion of biological facts in the context of Nei’s recent works, which ignore ecological factors and tout “constraint-breaking mutation” as the means by which mutation-driven evolution occurs.

Evolutionarily conserved molecules involved in the evolutionary scenario in sauropsids and in the life cycle of Drosophila orphan genes will probably be dismissed along with the biophysical constraints on ecological adaptations that are exemplified by the evolutionarily conserved molecules that promote differences in rat and human brain development. Nei, and others whose works are discussed, simply first ignore the biophysical constraints of ecological adaptations and then claim that “constraint-breaking mutation” is responsible for species diversity. The fact that no experimental evidence supports that claim will be of little concern to anyone whose social group pre-empts motivation for independent analytical thinking. “Ignorance is bliss” among social groups, isn’t it?

See, for example: Is America Evolving on Evolution? Feb 11, 2014 |By Sean B. Carroll

Sean B. Carroll, who thinks many people are not well-informed about evolution, subsequently co-authored an article in Science that refutes mutation-driven evolution by placing it into the context of ecological adaptations. My comment to the Science site on his latest publication may help others to realize how quickly researchers must change their reporting of cause and effect. They are forced to make it consistent with what is currently known about the nutrient-dependent pheromone-controlled ecological adaptations, which are clearly responsible for species diversity.

I hope others will someday join me in condemning Feierman’s despicable behaviors

This is the post Feierman edited for the human ethology group to prevent participants from becoming aware of what is known about the biology of behavior in species from microbes to man:

2/20/14

Feierman appears to be editing my posts . . . . . . editing my responses . . . and blocking some . . . . . . Other groups learn about what is currently known from sources that do not limit dissemination and discussion of accurate information . . . . . .  that refutes the theory of mutation-driven evolution . . . . . . Nei’s recent works that ignore ecological factors and tout[s] “constraint-breaking mutation” as the means by which mutation-driven evolution occurs . . .  Nei, and others, simply first ignore the biophysical constraints of ecological adaptations and then claim that “constraint-breaking mutation” is what is responsible for species diversity. The fact that there is no experimental evidence to support that claim will be of little concern to anyone . . .

What’s reported in this article seems to be exemplified among participants in the ISHE’s yahoo group. For example, Feierman appears to be editing my posts to ensure that the social structure of the group does not vary from how it has historically been maintained.

Participants collectively attack anyone with ideas based on independent analytical thinking, so that they can potentially oust an outsider who might otherwise force them to begin thinking analytically. Editing my responses to their attacks, and blocking some — but not all other — contributions, prevents participants from seeing how new data from experiments collectively supports ecological adaptation and refutes untested ideas about how natural selection might occur — if it occurred for anything other than food, as is required to meet one of Darwin’s ‘conditions of life’.

As some participants now know, however, preventing others from participating in discussions of how scientific progress is made via experimental evidence, ultimately fails. Other groups learn about what is currently known from sources that do not limit dissemination and discussion of accurate information.

For example, if Feierman were not editing and blocking some of my posts, we could now begin to discuss the fact that The life cycle of Drosophila orphan genes and Looking for the bird Kiss: evolutionary scenario in sauropsids and Embryonic Cerebrospinal Fluid Nanovesicles Carry Evolutionarily Conserved Molecules and Promote Neural Stem Cell Amplification fully support a model of ecological adaptations that refutes the theory of mutation-driven evolution.

Instead, participants will almost undoubtedly continue their discussions of theory and avoid discussion of biological facts in the context of Nei’s recent works that ignore ecological factors and tout “constraint-breaking mutation” as the means by which mutation-driven evolution occurs.

Evolutionarily conserved molecules involved in the evolutionary scenario in sauropsids and in the life cycle of Drosophila orphan genes can be dismissed along with the biophysical constraints on ecological adaptations that are exemplified by the evolutionarily conserved molecules that promote differences in rat and human brain development. Nei, and others, simply first ignore the biophysical constraints of ecological adaptations and then claim that “constraint-breaking mutation” is what is responsible for species diversity. The fact that there is no experimental evidence to support that claim will be of little concern to anyone whose social group pre-empts motivation for independent analytical thinking. “Ignorance is bliss” among social groups, isn’t it?

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We are all mutants!

February 19, 2014 | James Kohl

Discover Magazine 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. That biological fact should be embraced, cited and taught in schools. It seems that molecular evolutionary biologist Masatoshi Nei wants only mutation-driven evolution taught in schools. First he eliminated ecological factors in a 2011 journal article he co-authored: ‘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…” (p. 813)

In 2011 he did not consider ecological factors “because of space limitation.” In his book Mutation-driven evolution, he was concerned only with populations that were already ecologically isolated, which means they were already ecologically adapted. Nei again eliminated ecological factors. He wrote (with my emphasis):

“In this chapter, we first discuss the roles of chromosomal variation in speciation in the light of recent genomic data and then discuss various mechanisms of speciation by means of genic mutation and selection. We will consider both theories and experimental data that support or do not support a particular speciation model. We will be concerned only with the case of allopatric speciation, in which the populations to be differentiated are geographically or ecologically isolated. My primary purpose is to clarify the roles of mutation and selection in the evolution of reproductive isolation and show that the molecular basis of speciation is more complicated than generally thought at present.” (p. 138)

His primary purpose appears to be deception. In any attempt by serious scientists to clarify the idea of evolution, ecological factors must be considered. Serious scientists are not likely to believe anyone who tells them they are all mutants.

In my model, the ecological variability of nutrients is the determinant of ecological adaptations via the chemical ecology of ecological, social, neurogenic, and socio-cognitive niche construction. Nei tries to ensure that my model is not considered because it details how the epigenetic landscape becomes the physical landscape of DNA in the organized genomes of species from microbes to man without the involvement of mutations. But, in my model, there are examples of nutrient-dependent pheromone-controlled ecological adaptations. The examples clearly show there is no such thing as mutation-driven evolution. The biophysical constraints of protein folding make mutation-driven evolution a biological impossibility.

How does Nei manage to make it seem that mutation-driven evolution is biologically plausible? He eliminates ecological factors and evokes “constraint-breaking mutation.”

In Mutation-driven evolution, Nei wrote (with my emphasis):  “In other words, genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in the world. In the view of evolution there is no need of considering teleological elements.” (p. 199)

Why would someone like Nei not constrain himself from evoking nonsensical “constraint-breaking mutation” as the source of biodiversity in the world. Why would he first eliminate ecological factors, which are obviously the source of all the nutrient-dependent pheromone-controlled biodiversity in the world.

Has he lost his mind, or just escaped from academic constraints in an attempt to ride the wave of his reported expertise to his death?

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Metabolic insights make sense of ecological adaptations (revisiting Dobzhansky, 1973)

February 19, 2014 | James Kohl

Evolutionary history and metabolic insights of ancient mammalian uricases

Abstract excerpt: “Resurrected proteins reveal that ancestral uricases have steadily decreased in activity since the last common ancestor of mammals gave rise to descendent primate lineages. We were also able to determine the 3D distribution of amino acid replacements as they accumulated during evolutionary history…”

My comment: This is an important refutation of mutation-driven evolution. The refutation is based on models of climate change and diet change that lead to nutrient-dependent pheromone-controlled de novo gene creation, chromosomal rearrangements and ecological adaptations. The ecological adaptations occur with loss of genes and stabilization of the genome, which is manifested in the morphological and behavioral phenotypes of different species from microbes to man. See for example: Dobzhansky (1973) link opens PDF: Nothing in Biology Makes Any Sense Except in the Light of Evolution. This refutation of mutation-driven evolution shows us that nothing about evolution makes sense except in the light of biologically-based ecological adaptations.

Media report: Medical research February 18, 2014

Scarcity of fruit millions of years ago could have caused loss of enzyme that prevents gout

by Marcia Malory

Excerpt: “The researchers found that over time, mutations in the gene that codes for uricase made the enzyme progressively less effective. Finally, about 17 million years ago, apes developed a mutation that causes us not to produce any uricase at all.

The team noticed that the greatest reduction in uricase’s effectiveness took place when the Earth was cooling. From this, they hypothesized a connection between the decreasing ability to metabolize uric acid and an increasing scarcity of fruit.”

My comment: Climate change leads to changes in nutrient availability and natural selection of food via odors that epigenetically link the natural selection of food to metabolism of nutrients to the species-specific pheromones that control the physiology of reproduction in species from microbes to man.  No experimental evidence suggest that ecological variations in the food supply cause mutation-initiated natural selection, which is why the concept of natural selection for anything except food is falling out of favor with informed biologists. Predictably, we will next see the concept of mutation-driven evolution fall out of favor since all experimental evidence continues to provide support for species diversity that results from ecological adaptation.

See also:

A Resurrected Cretaceous Answer to the ‘Disease of Kings’

by Ed Yong

 Excerpt: “Uricase is an ancient invention, one that’s shared by bacteria and animals alike. But for some reason, apes have abandoned it. Our uricase gene has mutations that stop us from making the enzyme at all. It’s a “pseudogene”—the biological version of a corrupted computer file.”

My comment: We are biological creatures; not computers. For example, we must eat. Kratzer et al (2014) tested the alternative hypothesis associated with eating because mutations perturb protein folding. If they accumulate and perturb protein folding required for functional intercellular signaling, mutations are eliminated from the DNA of organized genomes in species from microbes to man. Also, mutations involved in gene expression are susceptible to compensatory changes that up-regulate expression of other genes. That masks epigenetic cause and effect, which is exemplified in the fact that “pseudogenes” are ever-present in the genome.

The pseudogenes are not eliminated from organized genomes. They remain in case their reactivation is required for more efficient nutrient-dependent intercellular signaling that may be required for organism level thermoregulation in ever-changing ecologies.  For example, olfactory receptor pseudogenes are not mutations that can be compared to “—the biological version of a corrupted computer file.”  The experience-dependent de novo creation of olfactory receptor genes exemplifies the flexibility that all genomes must maintain to respond to conditions of nutrient stress and social stress.

Some scientists and many science journalists fail to report results in terms of what is currently known about how the epigenetic landscape becomes the physical landscape of DNA.  Either they don’t know anything about current metabolic insights, or they choose to misrepresent cause and effect in the context of mutation-driven evolution. The misrepresentations of pseudogenes as corrupted computer files is akin to reporting science as if it were pseudoscience.

For comparison, the concluding paragraph of the discussion section in their publication, the co-authors state [subscription required]:  “In total, we have shown that ancient mutations decrease uricase activity over evolutionary time, and this progressive decrease is correlated with physiological function and (potential) adaptation.” The ecological adaptation is more efficient use of fructose (fruit sugar). Since no mutations were fixed in the genome, the correlation among 1) the presence of pseudogenes; 2) physiological function; and 3) adaptation, exemplifies one of many nutrient-dependent pheromone-controlled ecological adaptations, which are detailed in the context of the metabolic insights in my model.

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