“…epigenetic information carriers include covalent modifications to nucleotides and histones, providing a wide variety of mechanisms that enable organisms to transmit information extragenomically.”
When this was placed into its proper perspective, it was used in a parody by researchers who know how atoms and ecosystems are linked by RNA-mediated cell type differentiation in all living genera.
…it is important to be cautious in interpreting what this means for human health.
Sequencing both microRNA and mRNA enabled us to identify changes on the microRNA level, and also to investigate what is happening to gene expression at the mRNA level, to understand which pathways are activated or downregulated….
This link from the microRNA/mRNA balance to healthy longevity for comparison to virus-driven pathology may come as a surprise to evolutionary theorists and theoretical physicists who have no ideas about how biologically-based cause and effect MUST be linked from atoms to ecosystems.
Epigenetic mechanisms of inheritance December 1, 2015|
See for comparison: DNA Methylation: Insights into Human Evolution
Everything known to serious scientists who have linked atoms to ecosystems via nutrient-dependent RNA-mediated events and the physiology of reproduction in all living genera has been placed back into the context of evolution with the conclusion that
…the major challenge for the next years is to move beyond mere comparative descriptions and offer insight into phenotypic consequences. To that end, experimental assays are required.
That claim was made in Dobzhansky (1964):
The notion has gained some currency that 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!
Bacteria growing in an unchanging environment continue to adapt indefinitely. December 16, 2015|
…even in the absence of any external forces . . . evolution is going to be relentless nonetheless.
Like other researchers, he is confused about the difference between evolution and how ecological variation is linked to RNA-mediated ecological adapations like the nutrient-dependent pheromone-controlled “re-evolution” of the bacterial flagellum, which occurred over the weekend.
Serious scientists have since linked the conserved molecular mechanisms of cell type differentiaiton in microbes across species to humans via RNA-mediated amino acid substitutions in the context of cancer prevention and/or treatment.
Note that Louise Johnson of the University of Reading, U.K. reported that two mutations led to the re-evolution of the bacterial flagellum, when it was clearly two RNA-mediated amino acid substitutions that enabled the species to survive via ecological adaptation.
See the video.
Indications that GnRH peptide plays an important role in the control of sexual behaviors suggest that pheromone effects on these behaviors might also involve GnRH neurons. (p 683)
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).
DNA methylation is RNA-directed .When Roy Niles or anyone else has a model for comparison to mine, which links the conserved molecular mechanisms of nutrient-dependent RNA-mediated amino acid substitutions from atoms to ecosystems in all living genera, we can discuss other models in the context of intelligence and the ability to communicate effectively.
But first, serious scientists need an explanation of how weekend evolution of the bacterial flagellum occurred via trial and error. Is there a model for that?
Attempts to introduce serious scientists to the ridiculous philosophies that are based on the emergence of diversity in the gene pool are laughable now that all serious scientists know how to link atoms to ecosystems via biophysically constrained nutrient-dependent RNA-mediated protein folding chemistry that links the epigenetic landscape to the physical landscape of supercoiled DNA via microRNAs and cell adhesion proteins.
My comment: Physics, chemistry, and biology are linked from invertebrates to vertebrates via the conserved molecular mechanisms of nutrient-dependent RNA-mediated events and the pheromone-controlled physiology of reproduction in this brief representation of biologically-based cause and effect. In this example, the ecologically adapted vertebrate eats the invertebrate. The microbiome of the invertebrate is thereby linked to the microbiome of the vertebrate and to the vertebrate’s nutrient-dependent metabolism, which is linked to its pheromone-controlled physiology of reproduction via the conserved molecular mechanisms that link epigenetically-effected learning and memory to ecological adaptation from microbes to humans via the honeybee model organism.
The epigenetic effects of nutrients on intracellular signaling and stochastic gene expression appear to enable adaptive evolution of tightly controlled organism-level thermoregulation in mammals. Nutrient-dependent single amino acid substitutions and de novo protein biosynthesis exemplify the involvement of the seemingly futile thermodynamic control of intracellular and intermolecular interactions in microbes that result in stochastic gene expression.
Thermodynamically “futile” cycles of RNA transcription and degradation (Yap & Makeyev, 2013) may also be responsible for changes in pheromone production that enable accelerated changes in nutrient-dependent adaptive evolution controlled by the microRNA/messenger RNA (miRNA/mRNA) balance (see for review Meunier et al., 2013). Environmental cues, like those that signal the availability of glucose, appear to cause changes in the miRNA/mRNA balance that enable gene expression during developmental transitions required for successful nutrient-dependent reproduction in species from microbes (Park et al., 2010) to man (Jobe, McQuate, & Zhao, 2012).
My comment: The Ghosts in the Genome (above) can only be found in the context of thermodynamically “futile” cycles of RNA transcription and degradation linked from the epigenetic landscape to the physical landscape of supercoiled DNA by nutrient-dependent microRNAs and cell adhesion proteins that protect organized genomes from virus-driven genomic entropy in all living genera.
That fact links experimental evidence across all scientific disciplines to RNA-mediated cell type differentiation via the physiology of reproduction. No experimental evidence links the claims of evolutionary theorists to biologically-based cause and effect. That fact is admitted in the conclusion of: DNA Methylation: Insights into Human Evolution
Finally, the major challenge for the next years is to move beyond mere comparative descriptions and offer insight into phenotypic consequences. To that end, experimental assays are required. In this regard, humanized mice have proved useful resources [97,98]. However, they might not be suitable for interpreting certain phenotypes; perhaps induced pluripotent stem cells (iPSCs) could fill this gap . iPSCs can be differentiated to several cell types, providing a system in which to investigate the phenotypic effects of interspecies differences. We foresee an exciting decade for the field.
Experimental evidence that linked the mouse model of transgenerational epigenetic inheritance to human via the stability of supercoiled DNA established links from a single base pair substitution to a single amino acid substitution and receptor-mediated changes in morphological phenotypes linked to behavioral phenotypes in birds via nutrient-dependent pheromone-controlled chromosomal rearrangements.
The estrogen receptor polymorphism in the avian model has been linked to differences in other vertebrates by a single amino acid substitution.
For example, 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).
As he did in 1964, Dobzhansky portrayed cause and effect in the context of an amusing story about mutations and evolution.
The notion has gained some currency that 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! I have heard a man whose official title happens to be Professor of Zoology declare to an assembly of his colleagues that “a good man cannot teach zoology. A good man can teach, of course, only molecular biology.
Such pronunciamentos can be dismissed as merely ridiculous. They are, however, caricatures of opinions entertained by some intelligent and reasonable people, whose views deserve an honest and careful consideration and analysis. Science must cope with new problems that arise and devise new approaches to old problems. Some lines of research become less profitable and less exciting and others more so.
My comment: The less exciting works of pseudoscientists are a source of amusement for serious scientists who have tried to politely tell pseudoscientists that Dobzhansky was insulting their intelligence. Unfortunately, pseudoscientists cannot seem to understand anyone who politely tries to explain to them what is known about cell type differentiation, which only occurs in the context of atoms to ecosystems models.
For comparison to what a pseudoscientist might claim, serious scientists cannot start with de Vries definition of mutations as sudden energy jumps. Serious scientists are required to provide experimental evidence of biologically-based cause and effect that links the sun’s biological energy from Dobzhansky’s light of evolution via RNA-mediated events that differentiate all cell types of all living genera. The nutrient-dependent RNA-mediated events enable DNA repair and that prevents virus-driven genomic entropy, which is linked from de Vries definition of mutations to all pathology via the theft of nutrient energy by viruses.
Viruses steal the amino acids that cell types need to differentiate and perturb cell type function. Ultimately, a virus may cause a cell type to become a pluripotent undifferentiated cell type that steals all the nutrient energy from the cell for viral replication. But, if you tell that to a pseudoscientist, the virus-driven pathology will be linked from an amino acid substitution and reported as if the amino acid substitution caused the pathology.