A review of what we’ve learned about Creation in 2013
Excerpt: “These rare variants are so recent that they appear as novel mutations, with relatively little time for natural selection to operate.”
My comment: Rare variants are commonly referred to as mutations, which makes it seem to some people that the mutations were naturally selected. They are not mutations and they are not naturally selected. They are rare variants. Evolutionary theorists accepted Haldane’s idea of mutation-initiated natural selection without experimental evidence to support it. His idea became a widely-accepted theory. Now experimental evidence shows that mutations are not fixed in the genome of the nematode, C. elegans.
The fact that mutations are not fixed was made clear in An experimental test on the probability of extinction of new genetic variants.
Excerpt: “To our knowledge, this is the first time anyone was able to directly test Haldane’s theory. We have proved it correct for the initial stages, when a new allele appears in a population. But our results show that further empirical work and more theoretical models are required to accurately predict the fate of that allele over long time spans.”
My comment: Theorists seem unable to understand that no experimental evidence suggests that mutations are fixed in the DNA of any organized genome. Thus, no experimental evidence suggests mutations are naturally selected. The need for refined models of evolutionary cause and effect has been made clear above: “…our results show that further empirical work and more theoretical models are required…” Chelo et al (2013) might just as well have said that they had completely debunked the idea of mutation-driven evolution. But that would have invited a confrontation. Instead, other academics now try to use refined models of natural selection outside the context of mutations without saying what happened to mutation-driven evolution. Let’s see how that’s working for them, so far.
Excerpt: “In conclusion, we presented refined models of the recent explosive growth of a European population. These models can inform studies of natural selection (21, 39–41), the architecture of complex diseases, and the methods that should best be used for genotype-phenotype mapping.
My comment: How can “refined models” of population growth sans mutations be used to inform studies of natural selection? Mutation-driven evolution is gone from further consideration. Since mutations cannot be somehow selected, what is naturally selected in the refined models of recent explosive growth of a European population?
In my model, for example, food is naturally selected and selection epigenetically effects amino acid substitutions. There is experimental evidence of that biological fact. Is there any reason to not use my model and to keep refining other models of natural selection. Why can’t we all simply agree that natural selection is for food? Without food, nothing adapts; everything starves, it doesn’t evolve. For example, food effects transcription factor binding, which enables the de novo creation of new DNA.
Excerpt: “Our results indicate that simultaneous encoding of amino acid and regulatory information within exons is a major functional feature of complex genomes. The information architecture of the received genetic code is optimized for superimposition of additional information (34, 35), and this intrinsic flexibility has been extensively exploited by natural selection.”
My comment: But wait, I thought that food was natural selected. What was exploited? Are we supposed to still believe that something besides a mutation is naturally selected, and whatever that is also encodes transcription and simultaneously enables amino acid substitutions and de novo gene creation. I thought nutrient uptake facilitated amino acid substitutions, de novo gene creation, and increasingly complex cell types that are associated with ecological adaptation. Besides there’s a model for that.
There is also experimental evidence that nutrient-dependent pheromone-controlled amino acid substitutions differentiate all the cell types of all individuals in all species. For example: “… the epigenetic effects of food odors and pheromones are involved in neurogenic niche construction as exemplified in nematodes (Bumbarger, Riebesell, Rödelsperger, & Sommer, 2013), and in flies (Swarup et al., 2013).”
In 1996, we linked this experimental evidence to the molecular epigenetics of sexual differentiation at the advent of sexual reproduction in yeasts, which requires two different cell types that recognize their differences and “behave” appropriately based on the metabolism of nutrients to species-specific pheromones that enable the development of sexual orientation in reproductively mature cells.
Clearly, the indication that natural selection requires the selection of nutrients and that mutations are not naturally selected has been included in the extant literature since Dobzhansky (1964) Biology, molecular and organismic. Therefore, what once appeared to rare variants that appeared to be novel mutations can be examined in the context of Dobzhansky (1973): Nothing in Biology Makes Any Sense Except in the Light of Evolution.
For example, yesterday, I blogged about how Natural history replaces natural selection
Nutrient-dependent pheromone-controlled developmental staging and life history changes in a moth species: Manduca sexta takes us from the idea of what some of us were taught to believe was mutation-initiated natural selection by bird predation in the peppered moth. Some of us may have arrived at a point where we may accept the following accurate representation of ecological adaptations during the natural history of invertebrates, which is exemplified in all species. See, for example: Natural history-driven, plant-mediated RNAi-based study reveals CYP6B46’s role in a nicotine-mediated antipredator herbivore defense.
In this species, olfactory associations facilitate important life-history events, which are unrelated to the immediate foraging responses. Mutation-initiated natural selection cannot enable these associations with anything. Immature larvae become caterpillars that become moths sans mutations. Behavior is nutrient-dependent and pheromone-controlled during all stages of development. That fact is also exemplified in the honeybee model organism of ecological, social, neurogenic, and socio-cognitive niche construction. Simply put, the natural history of ecological adaptations replaces stories about natural selection.
In another blog post I wrote about the alernative scenario, where natural selection was eliminated and mutation-driven evolution “just happens”. But it doesn’t matter if natural selection was eliminated first or if mutations are only now being eliminated from the theory of mutation-initiated natural selection. Remember? There was never any experimental evidence to suggest mutation-initiated natural selection was possible.
Early today, I mentioned this: It has been fifty-five years since it became perfectly clear that nutrient-dependent pheromone-controlled ecological adaptation is responsible for hormone-organized and hormone-activated developmental differences in insects, but it seems there will be no end to the confusion about biologically based cause and effect in other species. That confusion was introduced via the theory of mutation-initiated evolution. See for example my post about the SICB 2014 meeting abstracts. It’s time to try to wrap up my thoughts for this year and move forward.
Excerpt: The knowledge of the chromatin signature of MAE [monoallelic expression] will help in exploring the relationship between MAE and functional cellular states in normal development and disease.
The monoallelic expression of newly created olfactory receptor genes is the singularity that represents the holy grail of evolutionary biology.
Eleven days after that blog post, we already have a way to link experience-dependent nutrient-dependent pheromone-controlled de novo creation of monoallelic olfactory receptor genes to monoallelic expression of other newly Created genes that differentiate cell types of different individuals of different species via natural selection of food.
The bottom line on this year’s discoveries is this: Ecological adaptation ensures that some genes are fixed in the DNA of organized genomes via the nutrient-dependent physiology of reproduction, which also helps to ensure that the majority of detrimental mutations are edited out during adaptations that lead to increasing organismal complexity. Thus, as an added benefit to acknowledging that my model of nutrient-dependent pheromone-controlled adaptations fits with what is known about de novo gene creation in all the different cell types of different individuals and different species, my model can be used to explore the relationship between nutrient excess, abnormal development, and disease.
I wonder if it will be.