Currently, there is no content. When content is added, it will almost undoubtedly further the cause of confusion that evolutionary theorists must use in attempts to prevent serious scientists from Combating Evolution to Fight Disease. Serious scientists use what is currently known about biologically-based cause and effect. Prepare yourself for more pseudoscientific nonsense about epimutations. Until then, see this:
…environmental factors are having an underappreciated effect on the course of disease and evolution by prompting genetic mutations through epigenetics, a process by which genes are turned on and off independent of an organism’s DNA sequence.
My comment: Food odors and pheromones epigenetically turn genes on and off via the conserved molecular mechanisms of biophysically constrained nutrient-dependent RNA-mediated protein folding. See for example: Signaling Crosstalk: Integrating Nutrient Availability and Sex and Human pheromones: integrating neuroendocrinology and ethology.
The molecular mechanisms are conserved in species from yeasts to humans as would be expected of links from physics to chemisty and to biology via molecular epigenetics. For contrast, misrepresentations of epigenetic cause and effect are attempts to “spin-doctor” the fact that ecological variation must lead to ecological adaptations in the context of virus-driven mutations. Spin-doctoring is required because virus-driven mutations have not been considered in the context of neo-Darwinian theories. That recently revealed fact makes the neo-Darwinian “Modern Synthesis” a unparalleled representation of pseudoscientific nonsense.
Serious scientists know that the anti-entropic epigenetic effects of nutrients on RNA-mediated gene duplication and RNA-mediated amino acid substitutions are required to differentiate all cell types of all individuals of all living genera.
Apparently, Michael K. Skinner still wants others to believe that the trangenerational epigenetic effects of environmental toxicants can be placed into the context of evolved biodiversity by linking DNA damage to biodiversity. Unfortunately for him, and other evolutionists, it has become clear that only RNA-mediated DNA-repair can be linked to biodiversity. Mutations perturb protein folding, which is how viruses are linked to pathology.
Although population geneticists predicted that stress-linked DNA damage could be linked to the evolution of biodiversity via mutations, generations of mutants cannot be linked by transgenerational epigenetic inheritance to the evolution of a different species. Only ecological variation and nutrient-dependent RNA-mediated DNA repair can be linked from ecological adaptations to biodiversity via the physiology of reproduction and fixation of amino acid substitutions. Fixation of the amino acid substitutions biophysically constrained by the chemistry of nutrient-dependent RNA-mediated protein folding.
“There’s not a type of genetic mutation known that’s not potentially influenced by environmental epigenetic effects,” Skinner said.
My comment: Attempts, like that, to make it appear the environmental epigenetic effects cause the mutations, are foolish. The environmental epigenetic effects of nutrients are the anti-entropic force that prevents genomic entropy via RNA-mediated repair mechanisms (e.g., nutrient-dependent RNA-mediated gene duplication and fixation of RNA-mediated amino acid substitutions, which stabilize the organized genomes of all genera.) See also: Feedback loops link odor and pheromone signaling with reproduction.
Excerpt (with my emphasis):
Erythrocyte DNA was obtained from five species of sympatric Darwin’s finches that vary in phylogenetic relatedness. Genome wide alterations in genetic mutations, using copy number variation (CNV), were compared with epigenetic alterations associated with differential DNA methylation regions (epimutations) (Skinner, et al. 2014b). A greater number of epimutations than genetic mutations was observed among the different species, with the number of epimutations increasing with phylogenetic distance. The number, chromosomal locations, regional clustering and overlap of epimutations suggests epigenetic change has likely had a role in the speciation and evolution of Darwin’s finches (Skinner, et al. 2014b). A number of additional observations also support a role of epigenetics and speciation. Using drosophila and maternally inherited noncoding RNA silencing of transposons a role for epigenetics and speciation was discussed (Brennecke, et al. 2008). The role of epigenetics and a punctuated equilibrium in the mobilization of transposable elements was also suggested (Zeh, et al. 2009). An interesting study comparing Neanderthal and human DNA methylation maps also supports a role for epigenetics in speciation (Gokhman, et al. 2014) and evolution.
Michael K. Skinner attempts to link nutrient-dependent RNA-mediated copy number variation (CNV) to evolution by placing them into the context of genome wide alterations in genetic mutations. After making it appear that CNVs are mutations, he attempts to make RNA-directed DNA methylation: an epigenetic pathway of increasing complexity synonymous with “epimutations” more than 40 years after Dobzhansky (1973) linked a single amino acid substitution to primate differences in hemoglobin, which is one of the proteins found in erythrocyte DNA.
…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).
Later this month, Michael K. Skinner will be attending this conference:
We will discuss both germ line and non-germ line modes of transmission and challenges for DNA methylation, microRNA and chromatin modifications as mechanisms of non-genomic inheritance.
The atoms to ecosystem model of ecological adaptation in my invited review of nutritional epigenetics links RNA-mediated DNA methylation and changes in the microRNA/messenger RNA balance to chromatin remodeling and biodiversity via chromosomal rearrangements.
There is no question about how non-genomic mechanisms of inheritance link science fiction to facts about RNA-mediated cell type differentiation that have been experimentally established during the past 30 years of scientific progress that linked this article “RNA-mediated gene duplication: the rat preproinsulin I gene is a functional retroposon” and Greg Bear’s accurate representations of biologically-based cause and RNA-mediated effect, which he summarized, non-technically in The Darwin Code.
My comment: Neo-Darwinian theorists have ignored these little happenings during the past 30 years. I wonder if anyone who knows how much pseudosceintific nonsense about epimutations has already been touted will be attending the conference that Skinner helped to organize.
It would be interesting to see a preliminary report issued before any of the likely collective misrepresentations of biologically-based cause and effect can be correlated. Typically, that’s what happens when attempts are made to make it appear that something meaningful has been accomplished by those who are now required to re-invent their ridiculous theories. See, for example: All in the (bigger) family. However, since then, Eugene Koonin admitted that none of the ridiculous theories included anything about the role of viruses in cell type differentiation.
This is a problem for anyone presenting at the conference: The entire evolution of the microbial world and the virus world, and the interaction between microbes and viruses and other life forms have been left out of the Modern Synthesis… –-Eugene Koonin (2015) from an interview with Suzan Mazur
For example: Brian Dias will present: “IMPRINTS OF ANCESTRAL OLFACTORY EXPERIENCE ON DESCENDANT GENERATIONS.” His most recent published work is: Epigenetic mechanisms underlying learning and the inheritance of learned behaviors
The fields of epigenetics and memory formation are in many ways natural complements of each other; however, they have historically been seen as altogether different events. How exciting and ironic if many of the mechanisms that underlie memory within an organism, and perhaps across generations, are due to these same epigenetic processes.
My comment The honeybee already serves as a model organism for studying human immunity, disease resistance, allergic reaction, circadian rhythms, antibiotic resistance, the development of the brain and behavior, mental health, longevity, diseases of the X chromosome, learning and memory, as well as conditioned responses to sensory stimuli (Kohl, 2012).
The history of that fact can be found in Organizational and activational effects of hormones on insect behavior and Honey bees as a model for understanding mechanisms of life history transitions.
My comment: Unless Brian Dias links the role of viruses to olfactory imprinting, it may be too late to spin-doctor any claims that do not integrate Koonin’s claim about viruses with this claim, which links the claims from the molecular epigenetics section of our 1996 review to everything currently known about nutrient-dependent RNA-mediated cell type differentiation via amino acid substitutions in all genera.
Genomic imprinting is a unique and long lasting form of epigenetic inheritance that relies on chromatin modifications or ‘imprints’ established in the parental germ lines and maintained in cells of the developing and adult organism, resulting in the differential expression of the maternally- or the paternally-inherited allele…
My comment: The transgenerational epigenetic inheritance of these alleles is nutrient-dependent and pheromone-controlled in all vertebrates and invertebrates via RNA-mediated gene duplication and RNA-mediated amino acid substitutions that are fixed in organized genomes via the physiology of reproduction in all genera. Mutations perturb the nutrient-dependent thermodynamic cycles of protein biosynthesis and degradation that link ecological variation to ecological adaptations in all genera.
It will be interesting to see what claims are made about epimutations in the context of links from metabolic networks to genetic networks, which have now been placed into the context of personalized medicine. Serious scientists may not like the idea of anyone inventing a term like “epimutation” in an attempt to continue the pseudoscientific nonsense that theorists have used to perturb the practice of medicine.
Serious scientists know that the practice of medicine must be based on how ecological variation and ecological adaptations are linked by Darwin’s conditions of life. Any remaining practitioners whose practice is based on population geneticist’s assumptions about how long it would take accumulated mutations to lead to the evolution of a new species should review the guiding principle to “First, do no harm.”
They could begin to review the literature that already links single amino acid substitutions to cell type differentiation during life history transitions in humans, like this report:
Will Michael K. Skinner attempt to link mutations or epimutations to life history transitions? Mutations perturb protein folding. What is an epimutation? How does a physician treat a mutation compared to treatment of an epimutation? How is an epimutation linked from biologically-based cause and effect to biodiversity? Is an epimutation the same as a paramutation?
Minoo Rassoulzadegan will present: “RNA-MEDIATED HEREDITY OF PARAMUTATION AND ACQUIRED PHENOTYPE IN THE MOUSE”
Clearly, Skinner and others like him are in over their head. The idea that any RNA-mediated event can be linked from a mutation, epimutation, paramutation, or anything else but nutrient uptake and the controlled physiology of reproduction is an idea that should have been eliminated from any further consideration whatsoever when Dobzhansky published: Nothing in Biology Makes Any Sense Except in the Light of Evolution
The evolutionary biologist Theodosius Dobzhansky famously noted that “nothing in biology makes sense except in the light of evolution,” but perhaps, too, “nothing in evolution makes sense except in the light of biology.” Although the latter might be an exaggeration, an important gap is being filled by molecular understanding of the genesis of variation that confers the ability to evolve.
The genesis of variation is nutrient-dependent and ecological variation is linked to ecological adaptation via the physiology of reproduction in all genera. The physiology of reproduction is perturbed by viruses that link entropic elasticity to genomic entropy due to stress, except when the anti-entropic epigenetic effect of nutrients on RNA-mediated cell type differentiation prevent the genomic entropy via fixation of amino acid substitutions that stabilize the organized genomes of all genera.
The stability of organized genomes can be re-evaluated in the context of claims about the “re-evolved” bacterial flagellum, which occurred over-the-weekend, and compared to the fossil record of bacteria that reportedly have not changed in ~2 billion years.
The reevaluation of claims about the time it might take for mutations to lead to the evolution of new species can now be compared to what is known about virus-driven changes, which were never before considered in the context of any atoms to ecosystems model of biodiversity.
So indeed, the new understanding of evolution needs to integrate what we now know about viruses and virus-host interactions which, from my own perspective, has been absolutely one of the key factors of all evolution since the emergence of cells — well, actually even before the emergence of cells.
Eugene Koonin thinks others should begin to integrate one of the key factors of all evolution, but that is what many others have been doing during the past two decades. What took so long for theorists to notice that others were questioning their ridiculous assumptions, which appear to be based on de Vries definition of “mutation” from the early 20th century.
See for comparison from the early 21st century:
Excerpt: It might also be necessary to develop models that allow patterns and rates of nonsynonymous evolution to differ among lineages. Although this will clearly add to the complexity of models, it may represent an important step toward reality; in the case of the primate lentiviruses, amino acid residues that are highly variable in HIV are sometimes conserved in chimpanzee SIV (19), and this may have a significant effect on dating estimates. Such lineage-specific differences in rate might be incorporated using the so-called “covarion” model of sequence change, which has a long history in molecular evolution (15) and is currently experiencing a newfound popularity (14, 16).