Excerpt: “A difference at the smallest level of DNA—one amino acid on one gene—can determine whether you find a given smell pleasant. A different amino acid on the same gene in your friend’s body could mean he finds the same odor offensive…”
My comment: In my model, the differences in the amino acids are caused by the epigenetic effects of nutrition on a single base pair. That’s how differences in nutrition cause differences in alternative splicings that lead to one amino acid substitution in the olfactory receptor genes of one person, and a different amino acid substitution in another person. Cause and effect is established via experience-dependent changes in base pairs, alternative splicings, and amino acid substitutions that differentiate individuals and species from microbes to man. For example, nutrient-dependent cause and effect, which results in amino acid substitutions and species diversity enabled researchers to determine the lineage of aquatic species related to the Ctenophore Mnemiopsis leidyi. That fact was reported in the December 13, 2013 issue of Science magazine. “The tree was produced from a matrix consisting of 242 genes and 104,840 amino acid characters.”
I published a review article in June, 2013, with details about how the amino acid substitutions can be used to explain all species diversification that has ever occurred. See: Nutrient-dependent/pheromone-controlled adaptive evolution: a model. However, the idea of epigenetically-effected amino acid substitutions and species diversity that is pheromone-controlled has only been publicly accepted by one person, Luke J. Terry.
He wrote: “My understanding of DNA’s data storage capacity is such that it’s not about the specific coding of nucleotides, e.g. the presence or importance of mutations, but emerges of the structure of DNA and the unique ways that DNA can be modified to create unique strings of information.” This understanding of cause and effect was provided in the context of the epigenetic effects of odors that alter amino acid substitutions and exemplify “…an information storage form for a string of…” amino acids that “…create unique proteins… as if it [DNA] were a code that could be used to encrypt… a string of pixels that make up a video…” Luke (who I just quoted/paraphrased) was responding to my post about this December 13, 2013 report in Science magazine. Exonic Transcription Factor Binding Directs Codon Choice and Affects Protein Evolution. Abstract excerpt: “Pervasive dual encoding of amino acid and regulatory information appears to be a fundamental feature of genome evolution.”
Luke’s response brings up this question: If genomes somehow evolve, what constrains their evolution so that we see similarities across species that appear to be based on conserved molecular mechanisms associated with ecological variation and amino acid substitutions? In a series of 799 blog posts here that began on December 12, 2010 with: Dialogue on pheromones: Avery Gilbert / James V. Kohl, I have repeated reasserted the fact that nutrients metabolize to pheromones, which control the physiology of reproduction in species from microbes to man. Those repeated assertions are based in a model of hormone-organized and hormone-activated behavior published in Hormones and Behavior in 1996: From Fertilization to Adult Sexual Behavior. That model linked the molecular epigenetics of alternative splicings to sex difference in species from unicellular yeasts to other multicellular primates via pheromone-controlled reproduction. No one has ever challenged any of the facts that we represented in that review, even though we did not clearly state that reproduction was nutrient-dependent. At the time, there was an opportunity to assert that sex differences were not nutrient-dependent, but the time for someone to suggest that mutations cause sex differences has passed.
Since then, Elekonich and Robinson (2000) “Organizational and activational effects of hormones on insect behavior“ extended the biological facts of nutrient-dependent pheromone-controlled species diversification to invertebrates. Five years later, Elekonich and Wilson (2005) Honey bees as a model for understanding mechanisms of life history transitions extended the invertebrate model to the model organism that they proposed would “… allow investigators to identify upregulation of receptors, enzymes and other functional components that coordinate CNS-based changes in thresholds for relevant stimuli… [and] … identify changes in the ability of sensory receptors to selectively perceive relevant changes in the environment…”
They predicted what the honeybee model organism has since shown: ”By measuring gene expression, endocrine, metabolic and neural physiology and behavior in groups of bees, future studies will be able to gain a detailed picture of how the distributed network of changes is integrated at the colony level.” Simply put, they predicted that nutrient-dependent pheromone-controlled amino acid substitutions would be manifested as species-specific variations among individuals and groups of organisms in every species. These variations result from ecological variation and the observable ecological, social, neurogenic, and socio-cognitive niche construction of increasing organismal complexity in species from microbes to man. Dobzhansky (1964) attributed the observable changes to mutations, but observable changes in organismal complexity are obviously are nutrient-dependent and pheromone-controlled. Dobzhansky(1964) also wrote 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!” (p. 443). Thus, even though there was not enough information about conserved molecular of amino acid substitutions for him to eliminate mutation theory from further consideration, he was correct to ignore, in advance, any additional reports from bird watchers or butterfly collectors (e.g., evolutionary theorists).
We know that Dobzhansky was not correct about mutations, but correct about the evolutionary theorists because, in yet another article from Science magazine that also was published on December 13, 2013, there is physical proof that observable changes in organismal complexity are nutrient-dependent. It has become apparent that epigenetic effects of nutrients on amino acid substitutions are observed in what is referred to as cryptic variation, which played a role in the evolution of eye loss in cavefish. HSP90 appears to be a capacitor for morphological evolution. However, only by reading a journalist’s report might others come to fully understand the role of this “so-called molecular chaperone”. It “…ensures proteins take on and maintain their correct shape, even if their amino acid sequence varies slightly because of mutations. By doing this for proteins important for development, the researchers proposed, HSP90 could theoretically hide the existence of accumulated mutations.”
If experimental evidence suggested that the complexity of any physical structure in any organism resulted from hidden accumulated mutations, there would be support for the theory that differences in the complex eyes of different species were caused by mutations. However, there is no experimental evidence that supports that theory. Now, experimental evidence has shown that eye regression is associated with changes in the amino acid sequence. Thus, even eye regression can be offered as an example of nutrient-dependent pheromone-controlled adaptation to the darkness of the caves.
The fish still need to eat, of course. But their ability to find food and mates is not linked to visual input. It might be linked to tactile input, as others concluded: “…the loss of eyes as a result of selection for increased tactile sensitivity is an attractive general hypothesis for the convergent evolution of eye regression in cave fauna.” However, vitamins also appear to act as molecular chaperones that transport amino acids from the intracellular environment to the intercellular realm of conserved molecular mechanisms in all cell types. Vitamins probably alter the thermodynamics of intercellular signaling that enables transcription, which we now know that DNA separates from gene expression.
Therefore, if nucleotide excision repair (NER) can remove many forms of DNA damage by nuclease cleavage on either side of the damaged bases, that fact would also exemplify what is known about how proper nutrition may epigenetically prevent deleterious mutations in different tissues in different individuals of different species that adapted to ecological variation with robust changes in morphology. Indeed, some experimental evidence suggests that “Enzymes and catalytic proteins have evolved to balance the thermodynamic challenges of stability and substrate throughput (Shoichet et al., 1995). Ion channels, for instance, must efficiently interconvert between open, closed and inactivated states to regulate ionic flux across biological membranes. Even small alterations in their function that change the rates of isomerization between states can underlie inherited or acquired diseases (Hille, 2001).” Predictably, receptor-mediated nutrient uptake alters the thermodynamic stability of intercellular signaling that biophysically constrains mutation-driven evolution. Biophysical constraints also promotes amino acid substitutions and transcription via the de novo Creation of amino acids that benefit an organisms survival, even if the organism is a blind cavefish that has already experienced amino acid changes that led to its eye regression. For example, the de novo Creation of olfactory receptor genes results in nutrient uptake and the metabolism of nutrients that enables the de novo Creation of species-specific pheromones in nematodes, as well as the de novo Creation of teeth in predatory nematodes, which is associated with their neurogenic niche construction and differences in their behavior.
This pattern has emerged from what is currently known about conserved molecular mechanisms:
1) Sex differences in cell types of yeasts are nutrient-dependent and pheromone-controlled
2) Other morphological differences in other species are nutrient-dependent and pheromone controlled
3) Amino acid substitutions are nutrient-dependent and pheromone controlled
4) Ecological, social, neurogenic, and socio-cognitive niche construction is enabled by amino acid substitutions that are nutrient-dependent and pheromone controlled
If I left anything out that might be associated with ecological variation and also be driven by mutations in all extant or extinct species that have ever existed on this planet, it would be interesting to learn more about what I have missed, provided it comes from experimental evidence to support the likelihood that I missed something important. As viewed from my perspective here, I do not think there is anything to be learned from theorists who have not tested their hypotheses by experimenting to see if their hypotheses make any sense whatsoever in the context of biological facts.