The comment I submitted on Thu 12/12/2013 about the findings below was published to the Science Magazine site on Tue 12/17/13 at 13:33
Science 13 December 2013:
Vol. 342 no. 6164
Excerpt: “This evolutionary framework, along with the comprehensive genomic resources made available through this study, will yield myriad discoveries about our most distant animal relatives, many of which will shed light not only on the biology of these extant organisms but also on the evolutionary history of all animal species, including our own.”
My comment: These findings are consistent with what is known about how ecological variation results in epigenetic changes, which are manifested in the amino acid substitutions. The amino acid substitutions differentiate species. Clearly, as I have said before: If you have variation, differential reproduction, and heredity, you will have what appears to be evolution by natural selection as an outcome. It is as simple as that. The variation is nutrient availability and nutrients metabolize to species-specific pheromones that control reproduction and heredity. Adaptations that occur via natural selection cannot be the outcome if something is not first selected. Selection is always for nutrients. It is as simple as that.
Species do not evolve via mutations; they adapt. Organismal complexity results from ecological, social, neurogenic, and socio-cognitive niche construction. That’s not as easy to understand as the comparatively simplistic mutation-driven evolution, but no experimental evidence supports the concept of mutation-driven evolution. As we see here, all experimental evidence supports the fact that ecological variation is the cause of adaptations associated with amino acid substitutions that establish biologically-based cause and effect, and refute theories of mutation-driven anything.
New findings reported: “The sequence of the M. leidyi genome has given rise to multiple categories of evidence that support the placement of ctenophores as the sister group to all other animals, a conclusion supported by phylogenetic analysis of amino acid matrices from concatenated protein sequences” (Ryan et al., 2013).
Predicted in “…the process of adaptation to the environment is the main propellant of evolutionary change. Evidence is rapidly accumulating which, in my opinion, substantiates the hypothesis. It remains, however, not only to convince the doubters but, what is more important, to discover just how the challenges of the environment are translated into evolutionary changes” (Dobzhansky, 1964, p. 451).
Refutation of mutation-driven evolution first established in the context of: “…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!” (Dobzhansky, 1964, p. 443).
With few exceptions, anything about evolution was placed into the context of mutation-initiated natural selection. “(1) Mutation is the source of all genetic variation on which any form of evolution is dependent. Mutation is the change of genomic structure and includes nucleotide substitution, insertion/deletion, segmental gene duplication, genomic duplication, changes in gene regulatory systems, transposition of genes, horizontal gene transfer, etc. (2) Natural selection is for saving advantageous mutations and eliminating harmful mutations. Selective advantage of the mutation is determined by the type of DNA change, and therefore natural selection is an evolutionary process initiated by mutation. It does not have any creative power in contrast to the statements made by some authors” (Nei, 2013, p. 196).
Even the change in the definition of mutation (above) does not divorce the theory of mutation-driven evolution from the lack of experimental evidence to support it. The problem is that no experimental evidence has ever shown that mutations are fixed in the genome of any species, and recent evidence has indicated fixation is unlikely because mutations are not fixed in the DNA of the organized genome of the model organism, Caenorhabditis elegans.(Chelo, Nédli, Gordo, & Teotónio, 2013)
Instead, there is now overwhelming evidence that the epigenetic landscape becomes the physical landscape of DNA in the organized genomes of species from microbes to man via nutrient-dependent alternative splicings and the amino acid substitutions provided in the article by Ryan, et al., (2013).
We can return to Dobzhansky’s oft-cited address to partially confirm the predictability that fixation of amino acid substitutions could be used to signal species-wide ecological adaptation. With other differences in amino acid sequences that vary across species, he noted that “…the so-called alpha chains of hemoglobin have identical sequences of amino acids in man and the chimpanzee, but they differ in a single amino acid (out of 141) in the gorilla”(Dobzhansky, 1973, p. 127). We can also examine the explanatory power of amino acid substitutions in the context of alternative splicings and their involvement in sexual differentiation in the unicellular yeast Caenorhabditis elegans, and in the multicellular invertebrate Drosophila melanogaster (see for review: Diamond, Binstock, & Kohl, 1996). These authors appear to have inadvertently or perhaps deliberately inferred that the amino acid substitutions were epigenetically fixed by the effects of species specific mammalian pheromones on gonadotropin releasing hormone.
The model of hormone-organized and hormone-activated behavior they detailed in the context of molecular epigenetics was extended to invertebrates by others (Elekonich & Robinson, 2000) and then to invertebrate life histories, which that exemplify both plieotropy and epistasis during critical periods of development associated with ecological, social, neurogenic, and socio-cognitive niche construction (Elekonich & Roberts, 2005).
Thermodynamically controlled intercellular interactions, stochastic gene expression, and organism-level thermoregulation of adaptations were extended from the mouse model to a population of modern humans in what is now central China. That population appears to have arisen during the past ~30,000 years in conjunction with the timing of a climate change that probably precipitated a change in their diet. The change in their diet probably caused the change in a single base pair that led to the amino acid substitution manifested in phenotypic changes. Those phenotypic changes were comparable to changes in the mouse model (see for review: Kohl, 2013).
Presumably, these changes are typical of what are now reported in the context of amino acid substitutions in other species (Ryan, et al., 2013), and differences in the amino acid substitutions of olfactory receptor genes in the olfactory receptor neurons of individual humans (Mainland et al., 2013. These authors concluded that “By assigning ligands to odorant receptors, measuring the functional consequences of segregating polymorphisms in vitro and linking in vitro function to human behavior, these data provide a solid platform from which to probe the effects of a single odorant receptor on olfactory perception (Mainland et al., 2013). They also appear to have inadvertently, albeit it tentatively, confirmed that the epigenetic landscape can be linked to the physical landscape of DNA in the organized genome of species from microbes to man via the effects of food odors and social odors on the de novo creation of olfactory receptor genes; the metabolism of nutrients and de novo creation of species-specific pheromones; the control of the physiology of reproduction by pheromones; and the de novo creation of teeth in predatory nematodes (Bumbarger, Riebesell, Rödelsperger, & Sommer, 2013) as well as the difference in morphology and behavior in species associated with the amino acid substitutions reported by Ryan et al., (2013)
See also: Perspective by Antonis Rokas Excerpt: This paints a picture of early animal evolution full of cell type complexity, as well as its loss.
See also the misrepresentation of these newly reported findings in In Search of the First Animals by Carl Zimmer. Excerpt: “A lot of our diseases may arise from damage to the fundamental system for building an animal that evolved some 700 million years ago.” My comment: Zimmer appears to believe that the association between mutations and diseases somehow causes mutation-driven evolution.
Bumbarger, Daniel J., Riebesell, M., Rödelsperger, C., & Sommer, Ralf J. (2013). System-wide Rewiring Underlies Behavioral Differences in Predatory and Bacterial-Feeding Nematodes. Cell, 152(1), 109-119.
Chelo, I. M., Nédli, J., Gordo, I., & Teotónio, H. (2013). An experimental test on the probability of extinction of new genetic variants. [Article]. Nat Commun, 4.
Diamond, M., Binstock, T., & Kohl, J. V. (1996). From Fertilization to Adult Sexual Behavior. Horm Behav, 30(4), 333-353.
Dobzhansky, T. (1964). Biology, molecular and organismic. American Zoologist, 4(4), 443-452.
Dobzhansky, T. (1973). Nothing in Biology Makes Any Sense Except in the Light of Evolution. American Biology Teacher, 35, 125-129.
Elekonich, M. M., & Roberts, S. P. (2005). Honey bees as a model for understanding mechanisms of life history transitions. Comp Biochem Physiol A Mol Integr Physiol, 141(4), 362-371.
Elekonich, M. M., & Robinson, G. (2000). Organizational and activational effects of hormones on insect behavior. J Insect Physiol, 46(12), 1509-1515.
Kohl, J. V. (2013). Nutrient–dependent / pheromone–controlled adaptive evolution: a model. Socioaffective Neuroscience & Psychology, 3(20553).
Mainland, J. D., Keller, A., Li, Y. R., Zhou, T., Trimmer, C., Snyder, L. L., et al. (2013). The missense of smell: functional variability in the human odorant receptor repertoire. [Article]. Nat Neurosci, advance online publication.
Nei, M. (2013). Mutation-Driven Evolution. Oxford, UK: Oxford Univesity Press.
Ryan, J. F., Pang, K., Schnitzler, C. E., Nguyen, A.-D., Moreland, R. T., Simmons, D. K., et al. (2013). The Genome of the Ctenophore Mnemiopsis leidyi and Its Implications for Cell Type Evolution. Science, 342(6164), DOI: 10.1126/science.1242592.