Summary: They link a single nucleotide polymorphism (SNP) to a genetic variant that decreases viability of an embryo, without linking a nutrient-dependent RNA-mediated amino acid substitution to pheromone-controlled cell type differentiation that begins in the embryo and continues throughout the life history transitions of invertebrates and vertebrates.
This genome-wide association study revealed “…a striking link between mitotic aneuploidy and a single nucleotide variant (SNP rs2305957) on chromosome 4 of maternal genomes.”
Excerpt: “There’s this genetic variant that they’ve been able to identify with very nice evidence for positive selection, but that has a fitness consequence, a fecundity consequence . . . that decreases the viability of an embryo,” said evolutionary geneticist Ed Green of the University of California, Santa Cruz, who was not involved in the work. “It flies in the face of what we think of in terms of positive Darwinian selection and demands an explanation.”
My comment: The “flies in the face” comment reminds me of a work from this same group on fertility in flies. Strong Purifying Selection at Synonymous Sites in D. melanogaster
Excerpt: “Regulation of gene expression may be acting at the level of mRNA structures, mRNA stability, miRNA binding sites, and the modulation of translation rate –.”
My comment: If so, fixation of nutrient-dependent amino acid substitutions can be linked to invertebrate cell type differentiation, but mutations, which are lethal or are not fixed, cannot be linked to biophysically constrained biodiversity. That attests to the fact that what most people think of in terms of positive Darwinian selection has no explanatory power. However, the thoughts of most theorists can be placed into the context of Dobzhansky’s claim: “…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” (p. 127). Nothing in Biology Makes Any Sense Except in the Light of Evolution
To make sense of how a single amino acid substitution in the developing embryo of a mammal or larvae of an invertebrate determines an organism’s fate, see also:
Section title: “3.1. mRNA of all intact VN1Rs is present in human olfactory mucosa”
See: 3.2. “Genetic variations of chemoreceptors caused by single nucleotide polymorphisms (SNPs) that result in an amino acid change…”
Wallrabenstein et al (2015) link what are obviously nutrient-dependent changes in the microRNA/messenger RNA (mRNA) balance to sexual differentiation of cell types and human communication with pheromones in adults. Greg Bear did this for a general audience in his science fiction novels “Darwin’s Radio” and “Darwin’s Children.” See, for example, this review of Darwin’s Radio.
In Kohl (2013) I wrote: “…ingested plant microRNAs influence gene expression across kingdoms (Zhang et al., 2012). In mammals, this epigenetically links what mammals eat to changes in gene expression (McNulty et al., 2011) and to new genes required for the evolutionary development of the mammalian placenta (Lynch, Leclerc, May, & Wagner, 2011) and the human brain…”
Simply put, ecological variation is linked to ecological adaptation that revolves around the conserved molecular mechanisms of nutrient-dependent RNA-directed DNA methylation and RNA-mediated events.
My model links RNA-mediated events to amino acid substitutions via natural selection based on food odors and the metabolism of nutrients to species-specific pheromones that control fixation of amino acid substitutions in the context of the nutrient-dependent physiology of reproduction. Chemical signaling among the rapidly differentiating cell types of embryos helps to ensure error recognition. If nutrient-dependent DNA repair mechanisms cannot immediately repair the errors that lead to perturbed protein folding, spontaneous abortion helps to ensure that the biological energy required to bring a mammalian pregnancy to a beneficial outcome is not wasted on a non-viable embryo.
For comparison to RNA-mediated biologically-based cause and effect that requires fixation of amino acid substitutions, when placed into the context of evolutionary theory, these “…findings seem “so paradoxical,” said Green, “I fear that any theory one can come up with is going to feel wrong in some way.”
I agree. Theories that fail to include what is known about RNA-mediated amino acid substitutions and cell type differentiation have no explanatory power. They will invariably be wrong compared to any model that incorporates what is known about top-down causation, which is that “Feedback loops link odor and pheromone signaling with reproduction.”
For comparison, see: Possible creatures by Andreas Wagner
Introduction: “It seemed Darwin had banished biological essences – yet evolution would fail without nature’s library of Platonic forms”
My comment: The number of possible creatures is nutrient-dependent and the biodiversity of all animal species is pheromone-controlled. Nutrient-dependent RNA-directed DNA methylation is linked to the diversity of cell types in all organisms of all species via the biophysically constrained chemistry of RNA-mediated protein folding.
Mutations perturb protein folding. Amino acid substitutions stabilize protein folding in organized genomes.
The biological essence of an organism is the stability of its organized genomes. That stability is linked from ecological variation to ecological adaptations by selection against mutations in species from microbes to man. Selection against mutations links the de novo creation of light-induced amino acids to RNA-mediated amino acid substitutions that differentiate all cell types in all genera.
The entropic elasticity attributed to viral microRNAs is linked from the anti-entropic energy of the sun to amino acid-dependent protein biosynthesis and degradation via everything currently known about physics, chemistry, and the conserved molecular mechanisms that Dobzhansky (1973) linked to cell type differentiation in primates via identical sequences of amino acids in man and the chimpanzee that differ in one single amino acid (out of 141) in the gorilla.
Alternatively, in theory: “…genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world. In this view of evolution there is no need of considering teleological elements.” Mutation-Driven Evolution (p. 199)
For comparison, see: “… the massive creative power of a cooperative RNA consortium (QS-C) remains crucial for life. QS-C was made known to us only recently by virus evolution (e.g., HIV-1). Its role in the origin of life, the emergence of complexity and the creation of group identity should now receive our combined attention.” Force for ancient and recent life: viral and stem-loop RNA consortia promote life (p. 8).
My comment: The likelihood that viruses “evolved” can be placed into the context of Andreas Wagner’s book: Arrival of the Fittest: Solving Evolution’s Greatest Puzzle and/or the context of creationist literature.
From an Editorial Review: Andreas Wagner presents a compelling, authoritative, and up-to-date case for bottom-up intelligence in biological evolution, and it sticks.’ — George Dyson, author of Turing’s Cathedral ‘
From the creationist literature: Viral Genome Junk Is Bunk “So, where do viruses come from that essentially share the same sequences as those found in their host genomes? Perhaps the evolutionists have placed the cart before the horse on this issue, as proposed by several creationist scientists.4,6 In fact, in an ironic twist, the evidence mentioned above indicates that viruses likely arose from their hosts and not the other way around. As molecular biologist and biochemist Peter Borger notes, “The most parsimonious answer is: the RNA viruses got their genes from their hosts.”6”
The questions arise: Did viruses “evolve?” Are changes in their virulence caused by “mutations?” How much longer will theorists be stuck with de Vries definition of “mutation” and the assumptions made by population geneticists about the time it might take for a different species to “evolve?”
Excerpt: “We cannot conceive of a global external factor that could cause, during this time, parallel evolution of amino acid compositions of proteins in 15 diverse taxa that represent all three domains of life and span a wide range of lifestyles and environments. Thus, currently, the most plausible hypothesis is that we are observing a universal, intrinsic trend that emerged before the last universal common ancestor of all extant organisms.”
See also: “There is a Corrigendum (26 May 2005) associated with this document. We have since discovered that a similar scenario for protein evolution was proposed by Zuckerkandl and colleagues more than thirty years ago1.”
My comment: It has now been nearly 45 years since publication of Mutational trends and random processes in the evolution of informational macromolecules.
Theorist who still can’t explain anything about how mutations might somehow be linked to the evolution of different species via differences in their life history transitions should ask: Why did Israeli middle schools begin teaching the theory of evolution last year? Serious scientists will understand this answer to that question: “…learning about evolution is not the primary function of the decision, but rather to use it as a building block for students to learn more about their ecology.”
Serious scientists are Combating Evolution to Fight Disease and they may be interested in recruiting intelligent combatants.
Creationists, it seems, have always been fighters. See also: Neo-Darwinism’s Catch-22: Before Evolving New Features, Organisms Would Be Swamped by Genetic Junk
Excerpt: “When it comes to generating viable living systems, it’s pretty much damned if you do, damned if you don’t. The bottom line seems to be that whatever cause generated the biological features we observe, unguided Darwinian evolution is not it.”