The evo-devo model. 2235 Words
DL noted that my model seems to be in tune with evo-devo (evolution of development) in the context of changes in regulatory processes, epigenesis, and the role of miRNA and mRNA etc, but that evo-devo relies on mutations to explain adaptive evolution. After correctly summarizing its content, he asked that I specify how my model of nutrient-dependent pheromone-controlled adaptive evolution leads to heritable DNA changes. He suggested it would be useful if I clearly described how age polyethism in Apis mellifera evolved sans mutations. I noted that the adaptive evolution of age-related differentiation of behavior (i.e., polyethism) had been detailed in accord with my published works.
JK: In the diagram of my model, you can “picture” what happens in vertebrates. There is no stage of life in mammals where epigenesis and epistasis are not epigenetically effected by food odors and pheromones. As detailed in From fertilization to adult sexual behavior, the mammalian model of hormone-organized and hormone-activated behavior was extended to invertebrates “from egg to adult” in Organizational and activational effects of hormones on insect behavior. Extension of the mammalian model to insects now includes well-studied mechanisms of age polyethism in the context of Honey bees as a model for understanding mechanisms of life history transitions. The link is to a review article that discusses physiological and genetic mechanisms of hormone-organized and hormone-activated behavioral transitions that include “…large scale changes in hormonal activity, metabolism, flight ability, circadian rhythms, sensory perception and processing, neural architecture, learning ability, memory and gene expression.” Gene expression in hormone-secreting nerve cells of brain tissue is the key indicator of cause and effect in my model.
DL: The article linked certainly has a wealth of detail on changes in gene expression that underlie age polyethism in bees. However doing a search within the article for “evol” (to find “evolve” or “evolution” etc) and “herit” (to find “inherit” or “heritable” etc) and “select” (to find terms related to selective forces) and “splic” (to find “alternative splicing/splice”) all fail to locate anywhere in the article where the authors discuss how change in gene expression or anything else might be transmitted to the next generation. As the authors argue, bees are certainly a great model organism for understanding the mechanisms of life history transitions within the lifetimes of worker bees (e.g., from being nurses that can barely fly to foragers that are great fliers), but that doesn’t address mechanisms of adaptive evolution. I noticed in another email you state that this article’s authors “Elekonich and Robinson used my model” but for some reason they do not cite “Kohl” in this article.
JK: Diamond, Binstock, and Kohl (1996) “From fertilization to adult sexual behavior” is consecutively cited twice in their “Background and history section” as Diamond et al., (1996)
1) “The development of species-typical and sex-specific adult behaviors in vertebrate animals is influenced by gonadal steroid hormones, non-gonadal hormones, and non-hormonal factors working on the underlying neural circuitry (reviewed in Diamond et al., 1996; Kawata, 1995; Schlinger, 1998).”
2) “Effects of hormones on brain and behavior occur through three mechanisms: (1) behaviors both organized and activated by hormones, (2) behaviors only organized by hormones, and (3) behaviors only activated by hormones (reviewed in Arnold and Breedlove, 1985; Diamond et al., 1996).” Simply put, Gene Robinson et al., have in the current century offered us a model organism in a series of articles that link nutrient-dependent pheromone-controlled development of behavior in all species.
DL: Life history transitions can be understood from the evo-devo perspective as having evolved to promote the adaptation of species members to their physical and social environments by properly timing and orchestrating developmental stages, which involves epigenetic processes that are consistently and reliably passed on to offspring. However, your frequent highlighting of “epigenetic effects on gene expression” is not accompanied by further explanation of how the different gene expression is presumably transmitted to the next generation. Does your model say that epigenetic effects actually change the genes? There’s some evidence that epigenetic marks might be transmitted to offspring or maybe even another generation or two, but that evidence is rare and contested (it seems rarer than the rate of potentially beneficial mutations). If epigenetic effects are at the heart of adaptive evolution, why isn’t there abundant evidence of this? It should be there, because biologists can currently identify and track epigenetic methyl and acetyl marks on genes in detail.
JK: Kohl (2012) incorporates the abundant evidence in species from microbes to man. For example, in Diamond, Binstock, and Kohl (1996), we indicated that alternative splicing was responsible for genetically predisposed nutrient-dependent pheromone-controlled Sexual Selection in our section on Molecular Epigenetics. This extends Natural Selection for nutrients to Sexual Selection for pheromones, as follows: “Yet another kind of epigenetic imprinting occurs in species as diverse as yeast, Drosophila, mice, and humans and is based upon small DNA-binding proteins called “chromo domain” proteins, e.g., polycomb. These proteins affect chromatin structure, often in telomeric regions, and thereby affect transcription and silencing of various genes (Saunders, Chue, Goebl, Craig, Clark, Powers, Eissenberg, Elgin, Rothfield, and Earnshaw, 1993; Singh, Miller, Pearce, Kothary, Burton, Paro, James, and Gaunt, 1991; Trofatter, Long, Murrell, Stotler, Gusella, and Buckler, 1995). Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to sexual differentiation in at least two species, Drosophila melanogaster and Caenorhabditis elegans (Adler and Hajduk, 1994; de Bono, Zarkower, and Hodgkin, 1995; Ge, Zuo, and Manley, 1991; Green, 1991; Parkhurst and Meneely, 1994; Wilkins, 1995; Wolfner, 1988). That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes.”
The small intranuclear proteins are now called microRNAs, and more than 2000 of them have been indentified (e.g., according to a Quiagen Webinar I listened to earlier today). It is the effects of the microRNAs on pre-RNA and sex differences, which appear to “…arise from alternative splicings of otherwise identical genes” that links nutrient-dependent pheromone-controlled adaptive evolution from the advent of sexual reproduction in yeasts to human sexual reproduction.
This is where evolutionary theory and mutations theory has failed. There is no indication from theory of how sex differences adaptively evolved. Perhaps I did not address this thoroughly when I indicated that my model “…must explain how alternative splicings lead to heritable changes in gene expression, and it does. See in From fertilization to adult sexual behavior,: “That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes.” If an alternative suggestion for the advent of sexual reproduction (and sexual orientation) has been proposed by evolutionary theorists, I haven’t learned of it.
DL: I used the same search terms within this Milton Diamond article and once again found that the various epigenetic influences and alternative gene splicings described only had to do with development over the course of a lifetime…..there’s nothing at all about how these lead to adaptive evolution.
JK: That review article is 16 years old; there are now more than 10,000 papers published on microRNAs, starting in 2002. Nevertheless, we clearly indicated it is the development of the sex differences over the course of a lifetime that leads to nutrient-dependent pheromone-controlled reproduction and genetic predispositions in offspring, which are the result of transgenerational epigenetic inheritance of genotypes that develop into activity-dependent stochastically determined phenotypes. For comparison, there is no indication from evolutionary theory of how mutations are selected that lead to sexual selection or to benefits in offspring.
DL: It’s beginning to sound like one key process for adaptive evolution in your model is the “alternative splicings of otherwise identical genes.” Does that mean that the solitary bees that gave rise to eusocial bees have essentially the same genes but the genes operate differently due to epigenetic marks and alternative splicings that have been acquired and passed on to successive generations?
JK: Yes! Thanks for posing that as a question, since you obviously knew the answer. I wrote: Natural selection for nutrients results in nutrient-dependent sex differences in pheromones that enable sexual selection for nutrient-dependent fitness in species from microbes to man. Berreby wrote: Research in behavioral epigenetics is seeking evidence that links experience to biochemistry to gene expression and back out again. Also: “It needs, and doesn’t yet have, at least one slam-dunk demonstration of all the links in a chain from behavior to neural activity to gene expression and back out again. How, for example, do biochemical events at a neuron’s nucleus affect the synaptic signaling between neurons that is the basis for all behavior?” I’ll make sense of this after I address your next comments and question.
DL: Although you use the Berreby article to support your model, the article actually seems to oppose it in the way it clarifies what “modern” epigenetics is about. Regarding what researchers in this field do, Berreby writes: “C.H. Waddington’s founding definition of epigenetics—transgenerational inheritance that isn’t dependent on DNA sequence—doesn’t fit what they do……Szyf thinks questions of heritability narrowly spotlight a single epigenetic time scale (what happens between generations), while methylation and demethylation occur at time scales ranging from seconds to hours (supporting short-term memories) to decades (supporting long-term memories), as well as generations. The emphasis on heritability is a cumbersome holdover from genetics, he says, ‘because in genetics, of course, everything is heritable. Do we want epigenetics to look like genetics? Why should we?'”
JK: What I want is for people to examine gene -x- environment interactions and realize that adaptive evolution is unequivocally dependent on genetically predisposed nutrient uptake/intake and the metabolism of nutrients to species specific pheromones, which is the only way the required reciprocity is established that links genes to behavior and back across species and transgenerationally – via the epigenetic effects of nutrients on Natural Selection and the epigenetic effects of pheromones on Sexual Selection. The epigenetic effects in vertebrates and invertebrates are hormone-organized and hormone-activated by food odors and pheromones.
Berreby asks: “How, for example, do biochemical events at a neuron’s nucleus affect the synaptic signaling between neurons that is the basis for all behavior?” In mammals, it is clear that MicroRNA-182 Regulates Amygdala-Dependent Memory Formation and that De novo mRNA synthesis is required for both consolidation and reconsolidation of fear memories in the amygdala. It is also clear that the molecular mechanisms for learning and memory are nutrient-dependent and pheromone-controlled in species where the microRNA / messenger RNA balance determines survival (e.g., epistasis). Simply put, if organisms cannot learn the difference between a food source and a conspecific, their species is not going to survive.
I wrote: I have since detailed how the required changes in gene expression occur but the details are not discussed. One antagonist continues to deny there is sufficient evidence of transgenerational epigenetic inheritance to dispense with the mutations theory. Others think that auditory and visual input directly activate “the physiological and genetic mechanisms of … behavioral transition[s], which include large scale changes in hormonal activity, metabolism, flight ability, circadian rhythms, sensory perception and processing, neural architecture, learning ability, memory and gene expression.” In the Psychiatry Research group, the idiot: Moonbat, poses ridiculous questions that show he knows nothing about the topic and that he has not read any of my published works. All others need to do is what you have done. Tell me what’s missing from my model. But what if it’s not! What if, for example, as I concluded: “Olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans.”
DL: Shouldn’t we expect that there must be an evolutionary trail from the common ancestor of all life, not only for olfaction and odor receptors but for all the other processes necessary for survival?
JK: Only nutrients are required for individual survival, and only nutrient-dependent pheromone production is required for reproduction and survival of species; for diversification of species via ecological and social niche construction, and for adaptively evolved intelligence via neurogenic and socio-cognitive niche construction. The evolutionary trail incorporates non-essential aspects of survival because other sensory input is associated with the epigenetic effects of food odors and pheromones. The associations are beneficial or species would not have incorporated them during adaptive evolution. However, in cave fish, when the visual association is no longer required, eye regression is the clearest indicator of the fact that visual input is not required for species survival in any species from microbes to man. Need I mention anything further about why “The Blind Watchmaker” theory of mutations and evolution seems ridiculous given the continuum of olfactory/pheromonal involvement but no continuum that includes eyes (or ears)?
Thanks again for facilitating answers to intelligent questions so others who are interested in comparing biological facts to theory might be encouraged to also ask intelligent questions. Clarence “Sonny” Williams will no doubt continue to advise others not to read my works, but to read others instead. Jay Feierman will continue to ignore my posts and block many of my responses on the ISHE human ethology group. John Angel and Glen Sizemore will do their best to berate me and promote animal training without acknowledging any current perspective on what is neuroscientifically known about classical conditioining compared to operant conditioining. And Moonbat will always be the anonymous fool. It will be interesting to see if anyone else asks questions about my model or the content of my published works in the context of scientific progress and epigenetic influences on the socioaffective nature of evolved behaviors, so that we can move forward from here.
