De novo creation of olfactory receptor (OR) genes links the material, physical and spiritual worlds (e.g., via Creation). See, for example with my emphasis, “A scenario thus emerges according to which neurons expressing ORs associated with environmentally salient odors are frequently active and may increase in relative abundance over time due to enhanced longevity, while neurons expressing infrequently activated ORs have a shortened life span, mediated in part by H2BE, and become less abundant (Figure 12). Differential longevity among olfactory sensory may provide an effective mechanism by which individuals with similar genomes adapt to diverse olfactory environments, facilitating enhanced sensitivity to odors important for survival.”
Q. Which odors are most important for survival?
A. Food odors and social odors, which are called pheromones.
If the scenario that has emerged (above) is true, the conserved molecular mechanisms that link species diversity to the de novo creation of olfactory receptor genes in species from microbes to man provide powerful examples of olfactory/pheromonal cause and effect. The examples are even more powerful because no examples have ever been offered that might otherwise support mutations theory, which has been touted as an explanation for evolution.
In the light of the scenario that has emerged (above), see my comment on what reviewers had to say about that report: Is what’s being elucidated the bottom-up epigenetic effects on stochastic gene expression via chromatin remodeling, which is controlled by the top-down epigenetic effects of pheromones on reproduction in species from microbes to man?
Lomvardas responded: “The article elucidates how the environment can broadly influence gene expression through an epigenetic effect chromatin – the way DNA is package and organized. This allows the environment to influence sensory function, to tune the olfactory sense to better suit the surrounding environment, because these environmentally regulated chromatin changes are coupled to cell longevity. This results in a change in the distribution of cells in the tissue that have made particular stochastic choices, where the stochastic choice is which olfactory receptor to express, without affecting the mechanism of stochastic gene expression.”
Yes! I said that’s what the article elucidated, except I phrased what they elucidated in more explicit terms of bottom-up cause and top-down regulated effect. Indeed, we addressed their elucidation, in part, in our 1996 Hormones and Behavior review article (in our section on molecular epigenetics): “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.”
More succinctly, alternative splicings contribute to the nutrient-dependent pheromone-controlled sex differences in the physiology of reproduction. That makes the epigenetic effects of odors (e.g., chemicals like food odors and pheromones) on alternative splicings, which contribute to the de novo creation of olfactory receptor genes, an extremely important consideration in the context of Creation and experience-induced nutrient-dependent species-specific reproduction controlled by pheromones.
But my reply to Lomvardas was blocked by the editor. Here’s the reply that was blocked: Thank you. In my model, the bottom-up epigenetic effects on stochastic gene expression are largely dependent on adaptively evolved glucose uptake and the top-down epigenetic effects on stochastic gene expression come from the metabolism of nutrient chemicals to species specific pheromones. The honeybee model organism best exemplifies this epigenetic tweaking of immense gene networks and how the epigenetic effects of food odors and pheromones on the glucose-dependent secretion of mammalian gonadotropin releasing hormone also links genes to behavior and back. The additional information about the histone core and fine-tuning of the required plasticity appear to attest to the control of chromatin remodeling by the microRNA / messenger RNA balance. It would interest me to learn if others agree with that proposal given the extreme technicalities of the issues addressed by Santoro and Dulac.
An eLife editor blocked my reply. He wrote: “We posted your first comment along with a response from the author but we have decided against posting your latest comment (below) because the discussion deviates away from the article in question. We also think it would be have been appropriate to declare your involvement with https://pheromones.com/”
What? My commercial involvement made my comment and my additional attempt to comment irrelevant after-the-fact. I got the impression that my comments were irrelevant because Lomvardas would not or could not address the first one in the context of his co-authored review. Two months later, this was accepted for posting to the eLife comments about the article: The activity-dependent histone variant H2BE modulates the life span of olfactory neurons
“I have since modeled nutrient-dependent pheromone-controlled adaptive evolution and uploaded the text and diagram, which are available here: https://dx.doi.org/10.6084/m9.f… I was advised I should have previously declared ownership of the domain Pheromones.com and my commercial involvement in marketing products based on animal models of common molecular mechanisms in species from microbes to man.”
Subsequent comments have been blocked. On 7/8/13, I wrote: “I own the domain Pheromones.com and recently published Kohl, J.V. (2013) Nutrient-dependent/pheromone-controlled adaptive evolution: a model. Socioaffective Neuroscience & Psychology, 3: 20553. This article details the bottom-up epigenetic effects on stochastic gene expression via chromatin remodeling, which is controlled by the top-down epigenetic effects of pheromones on reproduction in species from microbes to man. Across-species examples of nutrient-dependent pheromone-controlled adaptive evolution include a human population that arose in what is now central China during the past ~30,000 years. With other examples from model organisms, the human population helps to refute mutations theory, especially any theory about the role of ‘random’ mutations, because adaptive evolution is so obviously experience-dependent and controlled by nutrients from the bottom-up and controlled by the metabolism of nutrients to species-specific pheromones from the top-down.”
Note, there are still no example of cause and effect in the context of mutation-driven evolution. Thus, it remains unfortunate that, after the initial response by Lomvardas, who did not answer my question, the eLife editor did not allow me to post follow-up questions. Why? Was the problem my commercial interests , or could it have been a problem with academic interests? I think we will soon be seeing whose interests are at stake in the context of theory that can otherwise be compared to biological facts.
Evidence that mutations are not fixed in the genome of C. elegans can now be compared to evidence for olfactory/pheromonal control of the nutrient-dependent microRNA/messenger RNA balance that enables adaptive evolution in my model. This evidence can be extended across species via the model organism C. elegans, as we indicated it could be in our 1996 review. So can evidence for alternative splicings that lead to new alleles in Drosophila melanogaster. Indeed, our mammalian model of hormone-organized and hormone-activated vertebrate behavior was extended to invertebrates (flies, wasps, honebees, ants et al) in Organizational and activational effects of hormones on insect behavior. Organization and activation must somehow integrate new alleles that are fixed in the organized genome to enable species diversification sans mutations.
Giving credit to others, if it is due, I will first mention that the idea to include the importance of linking the epigenetic “landscape” to the physical landscape of DNA via alternative splicings in the organized genomes of species from microbes to man may have started with yeasts in our 1996 review. However, the idea may also have been fertilized or actually conceived in the minds of others who have since alluded to it using different phrasing. Clearly, the need for the epigenetic link from the sensory environment is known, especially since there is no experimental evidence to support mutation-driven evolution. For example, see:
Their goal, not yet reached, is to lay out every link in the causal chain that leads from a person’s experience to a neurotransmitter, then to a particular gene, then to a specific molecular modification of protein or DNA that affects that gene, and then back out from gene products to neuronal signaling to a person’s thoughts, feelings and actions. Published March 1, 2011
This was inspirational. I realized that others probably had missed the entire concept of olfactory/pheromonal effects via experience-driven changes in the hormone/neurotransmitter: gonadotropin releasing hormone (GnRH), in hormone secreting nerve cells of brain tissue that links experience directly to a person’s thoughts, feelings and actions. This gene-cell-tissue-organ-organ system reciprocity is essential to understanding biologically based cause and effect, and it has been the focus of my published works and presentations for more than 2 decades. For example, it was included in my 2012 review:
The concept that is extended is the epigenetic tweaking of immense gene networks in ‘superorganisms’ (Lockett, Kucharski, & Maleszka, 2012) that ‘solve problems through the exchange and the selective cancellation and modification of signals (Bear, 2004, p. 330)’. It is now clearer how an environmental drive probably evolved from that of food ingestion in unicellular organisms to that of socialization in insects. Published: March 15, 2012
That concept shows up, albeit only months to years later, in internet echos, like these:
“Thus, at the highest level of chromatin organization, the epigenetic ‘‘landscape’’ becomes a physical landscape where particular genes and regulatory sequences are hidden or exposed in accordance with the cell type and function.” Published: November 8, 2012
“A cell,” as Cole put it to me, “is a machine for translating experience into biology.” Published September 3, 2013
Meanwhile, what has happened with the theory of mutation-driven evolution? Clearly, it has not fared well in the context of Biological Information or in somewhat subtle attacks on theory that include aspects of how Physiology is rocking the foundations of evolutionary biology. These subtle attacks continue to introduce experimental evidence that could have been used to refute mutations theory at the first suggestion that the idea might ever be placed into the context of scientific pursuits. What we see now are clearer indications that mutations theory will not continue to be accepted by anyone who has ever mentioned the need to consider the sensory environment in the context of the conserved molecular mechanisms that epigenetically link olfactory/pheromonal input to adaptive evolution sans mutations theory. Epigenetics has resolved a problem of cause and effect that may infuriate some evolutionary theorists but inspire scientists to examine the biological facts rather than continue to accept a ridiculous theory that was never supported by any scientific experiment.
For experimental evidence of cause and effect, see also: Analysis of natural variation reveals neurogenetic networks for Drosophila olfactory behavior and Gene duplication as a mechanism of genomic adaptation to a changing environment.