From Fertilization to Adult Sexual Behavior (1996)
In our section on Molecular epigenetics, we wrote:
Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to sexual differentiation in at least two species, Drosophila melanogaster and Caenorhabditis elegans (Adler and Hajduk, 1994; de Bono, Zarkower, and Hodgkin, 1995; Ge, Zuo, and Manley, 1991; Green, 1991; Parkhurst and Meneely, 1994; Wilkins, 1995; Wolfner, 1988). That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes.
My comment: Serious scientists have since learned that all cell type differences arise from alternative splicings of otherwise identical genes. Pseudoscientists still make claims about the emergence of life and link natural selection to structural biology and the function of genome organization.
See for comparison: A Big Bang in spliceosome structural biology (2016)
Splicing cycles through a series of steps in which the spliceosome assembles on the intron-containing pre-mRNA, defining the boundaries between exons—the sequences ultimately retained in the mature mRNA—and introns (see the figure, panel A).
My comment: Energy-dependent changes in angstroms to ecosystems link the defined boundaries between exons and introns from ecological variation to ecological adaptation and all biodiversity. The “Big Bang” in structural biology is a contextualized polite way to tell theoretical physicists and other theorists that energy-dependent changes in functional structures must link ecological variation to ecological adaptation via what is known to serious scientists about all the links from angstroms to ecosystems in all living genera. Others have been trying to tell theorists how to link biologically-based cause and effect for several years.
See for example (2007): The MicroRNA miR-124 Promotes Neuronal Differentiation by Triggering Brain-Specific Alternative Pre-mRNA Splicing
Both microRNAs and alternative pre-mRNA splicing have been implicated in the development of the nervous system (NS), but functional interactions between these two pathways are poorly understood.
My comment: All serious scientists know that the functional interactions among microRNAs and alternative pre-mRNA splicing are nutrient energy-dependent and controlled by the physiology of reproduction. Do you know how energy-dependent RNA methylation links biophysically constrained protein folding chemistry to cell type differentiation via RNA-mediated amino acid substitutions? If not, you probably do not know why information about amino acid substitutions was left out of the claim that linked chromatin to the control of behavior in this misrepresentation:
Chromatin controls behavior
…the discoveries of Yang et al. are an important addition to an emerging literature implying a dynamic epigenome in the central nervous system (14, 15), which is contrary to the prevailing dogma in the epigenetics field.
My comment: There is no prevailing dogma in the epigenetics field. The dogma was eliminated when serious scientists linked energy-dependent changes from angstroms to ecosystems via epigenetic effects of sensory input on the innate immune system; the de novo creation of G protein-coupled receptors; the physiology of reproduction, and fixation of RNA-mediated amino acid substitutions that link supercoiled DNA to protection from virus-driven energy theft and genomic entropy in all organized genomes of all living genera.
See also: Chromatin remodeling inactivates activity genes and regulates neural coding.
Summary: Epigenetic regulation in the brain
The activity of neurons in the brain controls the transcription of genes that influence the pruning of dendritic connections between neurons, and such modifications can influence animal behavior. Yang et al. propose a role for chromatin remodeling by the nucleosome remodeling and deacetylase complex (NuRD) in the inactivation of such activity-dependent transcription in the mouse cerebellum (see the Perspective by Sweatt). Deposition of the histone variant H2A.z at promoters of activity-dependent genes required the NuRD complex. Loss of the NuRD complex function resulted in hypersensitivity of mice to sensory stimuli and excessive neuronal connectivity in animals performing a task on a treadmill.
This article was reported as: Ability to turn off genes in brain crucial for learning, memory
Excerpt (with my emphasis):
One process that controls chromatin structure and transcription is chromatin remodeling by energy-dependent protein complexes (4). Such complexes that depend on adenosine 5′-triphosphate (ATP) can control gene expression by moving, ejecting, or restructuring nucleosomes, the scaffolds around which DNA wraps. Each nucleosome contains a core particle of eight histone protein subunits (5). Remodeling events include posttranslational modifications, swapping individual One process that controls chromatin structure and transcription is chromatin remodeling by energy-dependent protein complexes (4). Such complexes that depend on adenosine 5′-triphosphate (ATP) can control gene expression by moving, ejecting, or restructuring nucleosomes, the scaffolds around which DNA wraps. Each nucleosome contains a core particle of eight histone protein subunits (5). Remodeling events include posttranslational modifications, swapping individual histone subunit isoforms into and out of the core particle, and facilitating the unbinding of DNA from the core particle.
into and out of the core particle, and facilitating the unbinding of DNA from the core particle.
My comment: Chromatin remodeling is energy-dependent. But, they buried the facts about how energy-dependent chromatin remodeling links sensory input from learning and memory to fixation of RNA-mediated amino acid substitutions. The substitutions differentiate all cell types of all individuals of all living genera, which explains why they invented the term histone subunit isoforms.
Serious scientists understand why pseudoscientists bury facts by stringing words together without telling others what a histone subunit isoform is, or what differentiates one histone subunit isoform from any other histone subunit isoform. In this case, the wordplay prevents others from learning that the availability of nutrients and nutrient energy-dependent changes links link fixation of RNA-mediated amino acid substitutions from learning and memory to chromatin remodeling and the control of behavior. Pseudoscientists tend to remove facts from consideration and remove the facts from the context of via well established pathways that link the epigenetic landscape to the physical landscape of supercoiled DNA in all living genera.
See for example: Roles of Mutation and Selection in Speciation: From Hugo de Vries to the Modern Genomic Era
…we will not consider geographical and ecological factors because of space limitation. Our primary purpose is to clarify the roles of mutation and selection in the evolution of reproductive isolation and show that the molecular basis of speciation is more complicated than generally thought at present. (p. 813)
My comment: Inventing the term histone subunit isoform outside the context of geographical and ecological factors is another way to dismiss the complexity of speciation.
See for example: This article mentions a subunit isoform in the context of Loss of the V-ATPase B1 Subunit Isoform Expressed in Non-Neuronal Cells of the Mouse Olfactory Epithelium Impairs Olfactory Function
The present study is the first to indicate the relevance of the VATPase, and presumably of V-ATPase-mediated proton secretion, in olfactory function. Undoubtedly, further functional and behavioral studies will allow a more comprehensive assessment of the physiological and clinical significance of V-ATPase expression in sustentacular and microvillar cells of the olfactory epithelium. At this point, we can only speculate on such possibilities. For example, modulating olfactory H+ secretion could offer the ability of up- or down-regulating the threshold of detection for certain odorants. Moreover, since the NML plays a role as a barrier against inhaled pathogens, and microbial and chemical toxins, regulating mucus pH may be relevant for protection against various specific diseases.
My comment: If you are unable to link the modulation of olfactory H+ secretion from hydrogen-atom transfer in DNA base pairs in solution to the de novo creation of G protein-coupled receptors and all energy-dependent biodiversity via RNA-mediated amino acid substitutions, please see:
Every amino acid matters: essential contributions of histone variants to mammalian development and disease.
The introduction of these minor sequence variants into chromatin is physiologically relevant and fundamental to eukaryotic cellular plasticity. However, with the exception of substitutions towards modification permissive amino acids (for example, both H3.1A31 and H3.2A31 to H3.3S31, which can be phosphorylated), it remains unclear how histone variants acquire and/or differentially enrich for specific chemical modifications that are distinct from their canonical counterparts.
My comment: They just muddied the perfectly clear waters of how phosphorylation and fixation of RNA-mediated amino substitutions is links from biophysically constrained protein folding chemistry to all biodiversity via hydrogen-atom transfer in DNA base pairs in solution. The claim that “every amino acid matters” is placed into the context of what is not known about biophysically constrained protein folding chemistry and biologically-based cause and effect. That is a way to help ensure these researcher get more funding. It’s a common tactic. If you focus on what is not known, people will think it’s not known to serious scientists who are funded to produce results that are supported by their experimental evidence of biologically-based cause and effect.
See also my comment on RNA and dynamic nuclear organization
Moving forward, if RNA-mediated events organize the cell nucleus, mutations manifested in perturbed protein folding are not likely to lead to natural selection and the evolution of biodiversity. The requirement for DNA to be found in organized genomes is biophysically constrained via the conserved molecular mechanisms of protein biosynthesis and degradation in species from microbes to man.
For simplicity, see:
See also: Structural diversity of supercoiled DNA and m1A and m1G disrupt A-RNA structure through the intrinsic instability of Hoogsteen base pairs, which was reported as:
My comment: The claim that DNA is the blueprint of life resurrects long-dead gene-centric theories. I expected others to make more rapid progress after the Zechiedrich lab linked energy-dependent changes from angstroms to ecosystems, but Al-Hashimi’s group is still reporting links in the context of pseudoscientific nonsense linked to neo-Darwinian theory. The theory does not address the need for biophysically constrained RNA-mediated protein folding chemistry in the context of the physiology of reproduction.
Perhaps Al-Hashimi’s group will be next to do that in RNA Structural Modules Control the Rate and Pathway of RNA Folding and Assembly, which supposedly is “In Press.” RNA methylation is clearly the link to all biodiversity. But, until then, they may fall behind even further, especially if they keep trying to placate the neo-Darwinists.
See: ‘Quantum jitters’ could form basis of evolution, cancer
“This is a remarkable study that illuminates a fundamental mechanism responsible for the random mutations that drive evolution and contribute to cancer,” said Bert Vogelstein, M.D., a cancer researcher at Johns Hopkins University School of Medicine who was not involved in this research.
My comment: How did Vogelstein arrive at his ridiculous conclusion? Did Visualizing transient Watson-Crick-like mispairs in DNA and RNA duplexes inadvertently or deliberately lead him to it?
These results, together with previous structural studies showing that WB and WC-like mispairs can exist within polymerase1–3 and ribosome5,6,13 active sites, strongly suggest that energetic competition between WB and WC-like mispairs is robust and is a key determinant of misincorporation probability during replication and translation (Supplementary Discussion 9).
My comment: How difficult would it have been to clarify the issues involved that suggest energetic competition causes the mutations, which means they do not randomly occur? I reiterate: Vogelstein thinks the “…study illuminates a fundamental mechanism responsible for the random mutations that drive evolution and contribute to cancer…”
Despite everything known to serious scientists about energetic competition for nutrients, I’m sure Vogelstein is not the only biologically uninformed cancer researcher who believes in neo-Darwinian theory. Others may also think that results framed in the context of energetic competition support ridiculous theories. Unfortunately, most people are not going to fight their way through an article like this one to discover that Vogelstein and all others like him are wrong.
Early myeloid lineage choice is not initiated by random PU.1 to GATA1 protein ratios
These observed protein dynamics are incompatible with random and cross-regulatory PU.1–GATA1 co-expression acting as the central mechanism that initiates MegE versus GM lineage choice3.
My comment: Most people may miss the fact that they claimed “…observed protein dynamics are incompatible with random… co-expression, which initiates lineage choice. Simply put, they eliminated Vogelstein’s ridiculous idea about random mutations from any further consideration.
See also: A miR-155–Peli1–c-Rel pathway controls the generation and function of T follicular helper cells, which was reported as A potential new way to sway the immune system found
“People know miRNAs are involved in immune response, but they don’t know which miRNAs and how exactly,” explained TSRI Research Associate Zhe Huang, study co-first author with Liu and Seung Goo Kang of TSRI and Kangwon National University.
In this experimental setting, the changes in the ratio of virus-transduced CD45.2+ cells (GFP+) versus WT competitors (CD45.1+) during the pro- to pre-B transition provided a measurement for the developmental defect. In the control WT:WT mix group, as no major difference existed between these two populations, the GFP+/CD45.1+ ratios remained unchanged during the pro- to pre-B transition, resulting in a pre-B/pro-B ratio close to 1 (Fig. 5b upper panels and Fig. 5c). In contrast, cells derived from the Mb1tKO HSCs, when transduced with control virus, underwent a severe developmental block in competition with WT cells. Therefore, the GFP+/CD45.1+ ratio shifted drastically as WT cells became dominant in the pre-B population, resulting in a pre-B/pro-B ratio below 0.2 (Fig. 5b middle panels and Fig. 5c).
My comment: All serious scientists know that nutrient energy-dependent microRNA flanking sequences link the innate immune system to differences in morphological and behavioral phenotypes via the physiology of reproduction in species from microbes to man via supercoiled DNA, which protects organized genomes of all living genera from virus-driven entropy.
Recent reports, which link specific families of miRNAs to healthy longevity or to pathology will obviously lead mroe researchers to discover the specific miRNAs that link virus-driven energy theft to all pathology.
See: The phylogenetic utility and functional constraint of microRNA flanking sequences and Role of olfaction in Octopus vulgaris reproduction
Future work on O. vulgaris olfaction must also consider how animals acquire the odours detected by the olfactory organ and what kind of odour the olfactory organ perceives. The OL acting as control centre may be target organ for metabolic hormones such as leptin like and insulin like peptides, and olfactory organ could exert regulatory action on the OL via epigenetic effects of nutrients and pheromones on gene expression (Kohl, 2013; Elekonich and Robinson, 2000).
See for comparison: (2016) Codon identity regulates mRNA stability and translation efficiency during the maternal-to-zygotic transition
The bias between codons or amino acids, and mRNA expression levels has been previously recognized across species and is thought to result from selection for efficient, accurate translation, and folding of highly expressed genes (Ikemura, 1982; Akashi, 1994; Akashi & Gojobori, 2002; Drummond & Wilke, 2008; Kudla et al, 2009; Novoa & Ribas de Pouplana, 2012). The amino acid optimality code (Fig 6) provides an alternative perspective on sequence changes between paralogs in evolution and human disease.
My comment: These authors echo the claim that random mutations are not the source of energy-dependent cell type differentiation. They add that the across-species bias of RNA-mediated amino acid substitutions offers an alternative to ridiculous claims about mutation-driven evolution. For another example of facts about RNA-mediated amino acid substitutions, see how Dobzhansky (1973) framed his claims.
…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).”
If you don’t like Young Earth Creationists, see also: (2016) Major Evolutionary Blunders: The ‘Degenerate’ Genetic Code?
A detailed literature review in 2014 found that even if different codons prescribed the same amino acid in a protein, the codon differences still mattered in how the protein was made. The final folding shape of proteins is vital to their function. David D’Onofrio and David Abel documented that the DNA and its corresponding RNA sequence carried information not only for the proper amino acid sequence but also to control the timing of its folding. They “demonstrate that this TP [translational pausing] code is programmed into the supposedly degenerate redundancy of the codon table.”8 What this means is that the code of differing codons, even if they specify the same amino acid, still supplies important information, information that “purposely slows or speeds up the translation-decoding process….Variable translation rates help prescribe functional folding of the nascent protein. Redundancy of the codon to amino acid mapping, therefore, is anything but superfluous or degenerate.”8
…if synonymous codons can have important functional meaning, then the whole methodology goes out the window, and hundreds of studies that used these methods to infer “selection” during the supposed “evolution of genes” could be wrong.11
If you like neo-Darwinian theorists, see: Tempo and mode of genome evolution in a 50,000-generation experiment
One line of evidence derives from the expectation that synonymous substitutions—point mutations in protein-coding genes that do not affect the amino-acid sequence—are neutral and should therefore accumulate at a rate equal to the underlying mutation rate20,35. This expectation is not strictly true owing to selection on codon usage, RNA folding, and other effects, but…
My comment: Let’s tell the truth with no buts, rather the invent more reasons to lie. Creationists and other serious scientists seem to arrive at the same conclusion by citing different literature that adds another level of epigenetic complexity in the context of non-random selection of RNA-mediated amino acid substitutions, which must be fixed in the organized genomes of all living genera to link the innate immune system to supercoiled DNA, which protects all organized genomes from virus-driven entropy.
The literature includes details about how the across species bias between codons or amino acids and microRNA or pre-mRNAs and mRNA expression levels links selection to efficient, accurate translation, and folding of highly expressed genes. For comparison, no serious scientist has ever suggested that virus-driven energy theft is linked from mutations and selection to the evolution of one species from another. Thus, it has become perfectly clear that the amount of pseudoscientific nonsense people must believe to continue to believe in mutation-driven evolution is based on definitions and assumptions. Serious scientists do not rely on definitions and assumptions to support their claims.
See for comparison: Mutation-Driven Evolution (2013)
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. —
In other words, 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.
[W]hat Haldane, Fisher, Sewell Wright, Hardy, Weinberg et al. did was invent…. The anglophone tradition was taught. I was taught, and so were my contemporaries, and so were the younger scientists. Evolution was defined as “changes in gene frequencies in natural populations.” The accumulation of genetic mutations was touted to be enough to change one species to another…. No, it wasn’t dishonesty. I think it was wish fulfillment and social momentum. Assumptions, made but not verified, were taught as fact.
For more assumptions in the context of ridiculous theories, see: Phylogenetic plasticity in the evolution of molluscan neural circuits (2016)
Molluscan neural circuitry represents a different evolutionary trajectory from vertebrates and even other lophotrochozoans. Using the same morphogenic genes as other phyla, molluscs have created novel nervous systems that control a wide variety of body forms. Yet the largest brained invertebrates, the cephalopods, have converged with insects and vertebrates on the organization of circuitry for learning and memory. Even with this cross-phyletic convergence, there are intra-phyletic differences between octopus and cuttlefish in the sites of plasticity. Phylogenetic plasticity is also found in gastropods where homologous neurons have been re-used for different functions and where neuromodulatory actions also display species-specificity. One outcome from this work is to show that there are many solutions to the same problem. The story of molluscs is about how looks can be deceiving; the same genes and neurons can be used and reused in different ways to create diverse nervous systems that sometimes converge on the same solution. I think it is more exciting to realize that octopus and mammals independently came up with a learning machine that has a fan-out/fan-in organization and LTP than to think that these similarities are just a family resemblance. Call me a splitter, but I believe that uncovering the many solutions that nature has found will tell us more about fundamental organizational properties than lumping them all together.
My comment: Anyone who makes a ridiculous statement like the one above should be ‘called out’ and questioned to learn how he or she has managed to maintain their overwhelming ignorance despite the availability of publications like this one:
The phylogenetic utility and functional constraint of microRNA flanking sequences and this one The octopus genome and the evolution of cephalopod neural and morphological novelties
Among the octopus complement of ligand-gated ion channels, we identified a set of atypical nicotinic acetylcholine receptor-like genes, most of which are tandemly arrayed in clusters (Extended Data Fig. 7). These subunits lack several residues identified as necessary for the binding of acetylcholine26, so it is unlikely that they function as acetylcholine receptors. The high level of expression of these divergent subunits within the suckers raises the interesting possibility that they act as sensory receptors, as do some divergent glutamate receptors in other protostomes27. In addition, we identified 74 Aplysia-like and 11 vertebrate-like candidate chemoreceptors among the octopus GPCR superfamily of ~330 genes (Extended Data Fig. 6).
My comment: The GPCR superfamily links receptor-mediated signaling from chemotaxis to phototaxis and all energy-dependent biophysically constrained biodiversity via RNA methylation and RNA-directed DNA methylation, histone acetylation and every aspect of the energy-dependent physiology of reproduction. Taken together, everything known about the energy-dependent receptor-mediated physiology of reproduction links the innate immune system to supercoiled DNA.
Those who tout neo-Darwinian theories for comparison must continue to use definitions and assumptions as if that approach was acceptable to anyone else who was not also a pseudoscientist.
See also: (2016) 33. Octopus Signals
We define a ‘signal’ as any act or structure which alters the behavior of other organisms, which evolved because of that effect, and which is effective because the receiver’s response has also evolved.
My comment: Via the bastardization of everything known to serious scientists about biologically-based cause and effect, the definition of signal is linked to its evolution via an effect, which is not linked from any epigenetic effect on hormones to any affect on behavior. That makes it impossible to link food odors to the energy-dependent de novo creation of olfactory receptor genes, which are GPCRs. The de novo gene creation of GPCRs links metabolic networks to genetic networks via the pheromone-controlled physiology of behavior in the context of epigenetic effects of pheromones on hormones. The hormones affect the species-specific behaviors of all invertebrates and vertebrates.
Definitions lead to confusion about the use of the terms “effect” and affect, which link epigenetic effects on hormones the the affects of hormones on behavior. Neo-Darwinian theorists skip everything known to serious scientists about the differences between effect and affect and link the definition of a ‘signal’ to species-specific behaviors and all biodiversity.
See for comparison: Feedback loops link odor and pheromone signaling with reproduction
It appears that GnRH neurons integrate a variety of information about the internal state of the animal and its external environment. At least 10,000 neurons in 26 different brain areas appear to transmit signals directly to GnRH neurons. Among these are areas involved in
odor and pheromone processing, sexual behavior, arousal, reward, and other functions. This suggests that GnRH neurons are poised to modulate reproductive physiology and behavior in accordance with the overall state of the animal.
These studies also indicate that GnRH neurons are likely to influence numerous brain functions. They appear to transmit signals to as many as 30,000 or more neurons in 34 brain areas, consistent with previous studies showing GnRH+ fibers and GnRH receptors in multiple brain regions (Badr and Pelletier, 1987; Jennes et al., 1988; Jennes et al., 1997). BL+ neurons likely to receive synaptic input from GnRH neurons were seen in areas associated with numerous different functions, including odor and pheromone processing, sexual behavior, appetite, defensive behavior, motor programs, and the relay of information to higher cortical areas. These results may reflect a strategy wherein GnRH neurons can modify diverse functions in order to coordinate the internal state of the animal and its behavior with reproduction in order to optimize reproductive success.
My comment: Have neo-Darwinian theorists found a species in which feedback loops do not link what the organism eats to its physiology of reproduction? If not, what do they claim links energy-dependent changes in angstroms to ecosystems in all living genera?
The 5300-year-old Helicobacter pylori genome of the Iceman
The “Iceman” H. pylori is a nearly pure representative of the bacterial population of Asian origin that existed in Europe before hybridization, suggesting that the African population arrived in Europe within the past few thousand years.
Glycans play many critical roles in both the normal function of cells and in disease. They assist in the folding of many proteins, aid in protein trafficking, mediate cell adhesion, differentiate blood groups, modulate the immune system, are implicated in many signaling pathways, and provide a protective extracellular matrix for many types of cells. Glycans are also implicated in the process of infectivity for many pathogenic bacteria (2) and most viruses (3), including those that cause the common cold, influenza, and HIV/AIDS.
Glycomics is now being used in combination with genomics, epigenomics, proteomics, lipidomics and metabolomics to provide a more holistic view of how cellular pathways function and how they change in response to disease.
It has become nearly impossible for me to keep up with the information that refutes neo-Darwinian pseudoscientific nonsense at the same time more articles are published that tout the nonsense.
See for comparison: The role of microRNAs in metabolic interactions between viruses and their hosts
Lineage tracing of human B cells reveals the in vivo landscape of human antibody class switching
… epigenetic inheritance of active and repressed chromatin state during mitosis has been demonstrated (Cavalli and Paro, 1998; Grewal and Klar, 1996). Our measurements suggest that the timescale on which the relative accessibility of IGHC loci persists is ~10 somatic mutations. Calibration of the mutational clock should allow recovery of information about epigenetic state and phenotypic dynamics in units of time and cellular generations. Together with recent studies of mammalian (Spencer et al., 2009) and bacterial cells in culture (Hormoz et al., 2015), our work suggests that phenotypic correlations between sister cells due to shared inheritance are widespread. We predict that such correlations often will be detected when genealogical relationships between individual cells can be resolved. We propose that inheritance of epigenetic state provides a mechanism for orchestrating cellular behavior without the need for signaling.
My comment: Attempts to define the term “signal” will fail because everyone knows what a signal is and all serious scientists know that food odors and pheromones are signals that link feedback loops from the innate immune system to chromatin folding and supercoiled DNA, which protects organized genomes from virus-driven entropy. The proposal the “…inheritance of epigenetic state provides a mechanism for orchestrating cellular behavior without the need for signaling” exemplifies the ignorance of all neo-Darwinian theorists who have failed to link energy-dependent signals to biophysically contrained protein folding chemistry via RNA methylation and RNA-mediated amino acid substitutions that differentiate all cell types in all individuals of all living genera.
Finally, see:Downstream Antisense Transcription Predicts Genomic Features That Define the Specific Chromatin Environment at Mammalian Promoters
It was reported on August 4, 2016 by Engaging Epigenetic Experts as:
…the authors say that they suspect such antisense transcription plays an important role in “in the regulation of gene expression and the maintenance of a promoter-associated chromatin environment.”
My comment: This site started removing my comments after several weeks of allowing me to accurately link articles like this one to what is known about RNA-mediated cell type differentiation. Others have already invented terms like oncohistones and histone subunit isoforms in attempt to continue obfuscating the links from energy-dependent RNA-mediated amino acid substitutions to healthy longevity because they know virus-driven energy theft has been linked to all pathology.
In the article mentioned by Engaging Epigenetics Experts, this claim is substantiated:
Despite differences in epigenetic features, tendency for association with transregulatory factors, and capacity to produce stable RNA transcripts, all three classes of TSS described in this work display similarities in sequence content, including enrichment for GC content and Pol II-associated sequence motifs (Fig 2). As such, antisense transcription appears to be encoded in genetic sequence. This connection between sequence content and epigenetic features provides the compelling suggestion that antisense transcription encoded by sequence may direct the positioning of nucleosomes and deposition of histone marks. Antisense transcription may also participate in signal-dependent modulation of epigenetic content where activation of sequence-encoded antisense TSS precedes nearby changes in chromatin structure. In this way, the collection of transcription initiation-associated sequence motifs near promoters may define regulatory potential for a given gene. This connection to sequence also provides a means to interrogate antisense transcription function. Future studies with selective mutation of associated sequence motifs may elucidate the function of antisense transcription and its coincidence with promoter-associated features. Directed mutagenesis could also establish the extent of the effect of antisense transcription on the chromatin environment at promoters.
We characterized downstream antisense transcription initiating near gene promoters in human T47D/A1-2 cells. daTSSs fall between regularly positioned nucleosomes downstream of gene TSSs. Histones within this region are enriched for marks closely associated with active promoter regions, such as H3K4me3 and H3K27ac modifications. Chromatin remodeling complexes show enriched binding upstream of observed daTSS positions, suggesting that antisense transcription contributes to the establishment and maintenance of a promoter-specific chromatin environment. Downstream antisense transcription is common to many human promoters, and daTSSs correlate with the downstream edge of promoter-associated chromatin features. Coincidence of daTSSs with these features suggests interplay between antisense transcription and regulatory pathways.
My comment: There are too many ways to obfuscate what is known about the epigenetically-effected links from energy-dependent changes in angstroms to ecosystems in all living genera. These two paragraphs are important to understand in that context. They link RNA methylation and RNA-mediated amino acid substitutions to cell type differentiation in all living genera via chromatin remodeling, but you will not be encourage to look at the facts because there is no mention of epigenetically-effected RNA-mediated amino acid substitutions in the context of chromatin remodeling. That’s why I added emphasis to this claim: “…transcription initiation-associated sequence motifs near promoters may define regulatory potential for a given gene.”
It links hydrogen-atom transfer in DNA base pairs in solution from energy-dependent changes in the microRNA/messenger RNA balance to gene regulation via everything known to serious scientists. It links RNA-mediated amino acid substitutions and morphological diversity by linking energy-dependent RNA methylation from learning and memory to behavior via chromatin remodeling. The chromatin remodeling occurs in the context of the physiology of reproduction and what is known about supercoiled DNA, which protects all organized genomes from virus-driven energy theft and genomic entropy.
But their claim that “…transcription initiation-associated sequence motifs near promoters may define regulatory potential for a given gene” is placed into the context of a theory about the fact that energy-dependent RNA-mediated amino acids substitutions, which are referred to in the context of transcription initiation-associated sequence motifs may define the energy-dependent regulatory potential of different genes in different individuals of different species. All pseudoscientists know how to obfuscate facts about the energy-dependent regulatory potential of different genes, because they have been placing them into the context of virus-driven energy theft and mutation-driven evolution since the time that de Vries (1902) defined “mutation.”
Addendum: People complain that I am not explaining how quantum physics, quantum chemistry, quantum biology, and quantum consciousness in terms they can understand. See:
Real-world explanation: Brian Greene : What’s Beyond The Double Slit Experiment ?
Our Reality Is Information Tom Campbell
Probability & Uncertainty: The quantum mechanical view of nature Richard Feynman
New Experiments Show Consciousness Affects Matter Dean Radin