“You don’t own the knowledge.”
My comment: Researchers own nothing without patents based on the knowledge. They do not own the knowledge that leads others to learn more about what has been accurately portrayed in the context of biophysically constrained biologically-based cause and effect.
Tomi Aalto is correct. Any biologically uninformed layperson or scientist who makes a living by stealing the knowledge from others can do that without fear of litigation. That’s why misrepresentations about what is known have led to delayed understanding about the role of energy and virus-driven energy theft in RNA-mediated cell type differentiation.
Simplistic theories about mutations and evolution have prevailed.
For comparison, the systems complexity of energy-dependent RNA-mediated cell type differentiation and virus-driven energy theft linked to all pathology is overwhelming.
…specific tRNAs can form ‘‘inducible’’ pathways with their direct target transcripts, which are enriched for their cognate codons. Such target transcripts can become stabilized in the context of their favored tRNA content or can be more effectively translated—ultimately yielding greater protein output.
My comment: The stability of the target transcripts is energy-dependent and controlled by the physiology of reproduction, which links metabolic networks to genetic networks via RNA-mediated amino acid substitutions and supercoiled DNA, which protects all organized genomes from virus-driven energy theft and genomic entropy. That is the fact that people like Tomi Aalto want to portray as if they came to their conclusions based on their “raw insight.” It is a fact that people like Sean Ovis want to portray as if it did not refute the pseudoscientific nonsense of neo-Darwinian evolution.
The fact was reported as: Researchers uncover how “silent” genetic changes drive cancer
[It] challenges previous assumptions about how tRNAs function and suggests that tRNAs can modulate gene expression, according to the researchers. Tavazoie points out that “it is remarkable that within a single cell type, synonymous changes in genetic sequence can dramatically affect the levels of specific proteins, their transcripts, and the way a cell behaves.”
My comment: They have indirectly linked energy-dependent RNA methylation to what they place into the context of “…the way a cell behaves.” This makes it appear that cancer cells are nothing more than cells that behave badly. The cause of their “bad behavior” is not addressed for comparison to the behavior of differentiated cells that contribute to the energy-dependent healthy longevity of species from microbes to humans.
The emerging correlation between miRNA expression and disease pathogenesis and outcomes suggests the potential use of miRNAs as biomarkers. In the first report that described the role of a miRNA as a diagnostic and prognostic marker in humans, Takamizawa et al. demonstrated that in patients with lung cancer, lower let-7 levels predicted a significantly worse prognosis after potentially curative resection (6).
My comment: I continue to wonder why virus-driven energy theft is not considered in the context of nutrient-dependent pheromone-controlled biodiversity, which links the morphological and behavioral phenotypes of microbes from insects to primates.
See for comparison: Subcaste-specific evolution of head size in the ant genus Pheidole
A recent study of global Pheidole demonstrated that body size variation was similar in Old and New World species, and that Pheidole communities repeatedly evolve similar size distributions despite inhabiting a range of biomes (Economo et al., 2015). These results also imply strong constraints on body size evolution. Future work at community scales is still needed to determine whether Pheidole species assemblages show divergence in morphology with respect to diet partitioning (e.g. to escape competition).
My comment: Biophysically constrained energy-dependent ecological adaptations link differences in ants to differences in primates. They also link virus-driven energy theft to the Dutch famine.
“We found four basic gene sequences in P. andina that are a close match to the variant that caused the famine in the 1840s. Our analyses also show that P. andina and the historical variant of P. infestans split into two distinct groups before the modern Mexican varieties developed,” says Martin.
In layman’s terms, this means that the disease may have originated in the Andes earlier than variants of the disease evolved in Mexico.
Does that give us a definitive blueprint? No, not really, but it does cast doubt on the idea that Mexico is the site where the disease originated. It also confirms that the evolutionary history of blight is very complex. We need to know more.
And although Martin recently completed his time in Copenhagen, he is continuing his research on blight.
NTNU has awarded Martin a tenure-track position as part of the Onsager Fellowship Programme, which recruits young, outstanding researchers to strengthen the university.
My comment: The strength of many universities is based on pseudoscientific nonsense like he will be touting because he does not know that de novo gene creation is energy-dependent and that virus-driven energy theft caused the potato blight.
…there was a reason, and it was called the Tulip Breaking Virus, or mosaic virus. It was transmitted either by contact with the bulb of an infected tulip or by different species of aphids. It changes pigmentation by affecting the distribution of anthocyanin, a pigment that can appear different colors depending on the pH of its area.
My comment: The inability of most mainstream scientists to link Rosalind Franklin’s works with the tobacco mosaic virus to her questions about the representations of a static DNA double helix should by now have been attacked with experimental evidence that links energy-dependent changes from angstroms to ecosystems. The Zechiedrich lab may need to stop poking fun at others and tell them to stop touting pseudoscientific nonsense about mutations and evolution. It seems likely that anyone who is currently combating evolution to fight disease may need to help attack the neo-Darwinian theorists.
Unless all serious scientists attack, there may be no end to the pseudoscientific nonsense touted by evolutionary theorists.
See for example: New faculty member investigates how genes are born and proliferate
“It has recently become clear that new genes can arise from DNA that previously did not code for protein, and that each species has a set of genes that is uniquely its own,” says Dr. Zhao, who is currently a postdoc at the University of California, Davis. “I am interested in examining how these genes originate, spread, and contribute to the adaptation of populations to their environment.”
My comment: Quantized energy as information is linked from the epigenetic landscape to the physical landscape of newly created genes by two epigenetic traps that link supercoiled DNA to protection of all organized genomes from virus-driven energy theft in the context of the energy-dependent physiology of reproduction.
See also: Drosophila’s New Genes January 23, 2014
The de novo creation of genes has previously been reported to be the “holy grail” of evolutionary biology. If that is true, what’s reported here exemplifies the fact that the “holy grail” involves only the direct olfactory/pheromonal link from the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man.
See, for example, our 1996 Hormones and Behavior review article: From Fertilization to Adult Sexual Behavior (e.g., the section on molecular epigenetics where TB 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…”
The alternative splicings are obviously nutrient-dependent and they lead to 1) de novo gene creation and 2) chromosomal rearrangements, which are exemplified in sex diffferences at the advent of sexual differentiation in the cell types of yeasts that sexually reproduce. The physiology of reproduction is controlled by the metabolism of nutrients to pheromones in species from microbes to man. That means de novo creation of genes probably occurs via conserved molecular mechanisms in all species (see: Organizational and activational effects of hormones on insect behavior).
Alternatively, mutation-driven evolution can be substituted for the nutrient-dependent pheromone-controlled ecological adaptations that enable species divergence. Theorists need only explain how natural selection for mutations occurs so that their theory can be compared to a model of ecological variation and natural selection of food.
The model incorporates what is required for the Creation of new genes that enable organismal complexity via ecological, social, neurogenic, and socio-cognitive niche construction. What’s required is food and nutrient-dependent pheromone-controlled reproduction. See for example: Nutrient-dependent/pheromone-controlled adaptive evolution: a model
This is a hypothesis-driven manuscript, so we have had our limitations in terms of finding desired published literature. We, however, think that there is a possibility of moving towards the identification of a non-invasive diagnostic biomarker for PCa and/or aggressive PCa by quantifying circulating miR-150. The core idea of miR-150 being bioaccumulated and interspecifically transferred is also vital for the identification of a possible therapeutic biomarker for PCa, as we believe that we are what we eat.
The senior author, Lynnette Ferguson was one of the two guest editors for a special issue of “Nutrients.” After I published: Nutrient-dependent/pheromone-controlled adaptive evolution: a model Justin M. O’Sullivan and Lynnette Ferguson asked me to submit an invited review of nutritional epigenetics.
See also the logical extension of this model to: Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems
This atoms to ecosystems model of ecological adaptations links nutrient-dependent epigenetic effects on base pairs and amino acid substitutions to pheromone-controlled changes in the microRNA / messenger RNA balance and chromosomal rearrangements. The nutrient-dependent pheromone-controlled changes are required for the thermodynamic regulation of intracellular signaling, which enables biophysically constrained nutrient-dependent protein folding; experience-dependent receptor-mediated behaviors, and organism-level thermoregulation in ever-changing ecological niches and social niches. Nutrient-dependent pheromone-controlled ecological, social, neurogenic and socio-cognitive niche construction are manifested in increasing organismal complexity in species from microbes to man.
My comment: My invited review was returned without review by Justin M. O’Sullivan and Lynnette Ferguson, which explains why Ferguson’s group claims “This is a hypothesis-driven manuscript, so we have had our limitations in terms of finding desired published literature.”
My review of nutrient energy-dependent RNA mediated cell type differentiation had been published, I might have moved forward with the obvious link from virus-driven energy theft to all pathology, which I have since established in a series of poster presentations. Justin M. O’Sullivan and Lynnette Ferguson are only two of the academically untalented and biologically uninformed researchers I have encountered whose despicable behaviors are common. They have no choice but to use the ideas and works of others in attempt to make gains without making the effort that is required to integrate the information across disciplines.
See for comparison: Vast Complexity of Immune Micro RNA Signals Jon Lieff has been following in my footsteps since the time I commented on this representation of: Alternative RNA Splicing in Evolution
In our 1996 Hormones and Behavior review, 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.”
The alternative splicings are nutrient-dependent and appear to be enabled by the experience-dependent de novo creation of olfactory receptor genes, which enable additional receptor-mediated nutrient uptake and the metabolism of nutrients to species-specific blends of pheromones that control reproduction in species from microbes to man.
Your focus on the importance of pre-mRNA and alternative splicing is exemplary, especially in the context of neuronal plasticity.
C. elegans is the model organism of neurogenic niche construction that links nutrient-dependent ecological and pheromone-controlled social niche construction to socio-cognitive niche construction in vertebrates and invertebrates. See for review:
What you are helping to detail is self-assembly with evidence of olfactory/pheromonal self-organization that is currently missing from evolutionary theory, which attributes speciation to mutation-initiated natural selection even though there is no experimental evidence for that (as I mentioned elsewhere).
…while scientists used to think the RNA was just a ‘middleman’, they’ve realised over the past few decades that it does so much more than that – it can control which proteins are produced in the cell.
Excerpt: They have previously used this tool to remove HIV from human immune cells and shut down HIV replication permanently, according to a study published in Nature in March.
Excerpt: “Mutation in the HER2 gene favors the growth of cancer cells.”
My comment: Virus-driven energy theft causes all mutations.
The ability to design extensive hydrogen-bond networks with atomic accuracy enables the programming of protein interaction specificity for a broad range of synthetic biology applications; more generally, our results demonstrate that, even with the tremendous diversity observed in nature, there are fundamentally new modes of interaction to be discovered in proteins.
My comment: The ability to link energy-dependent changes hydrogen-atom transfer in DNA base pairs in solution from microRNA flanking sequences to adhesion proteins and supercoiled DNA that protects all organized genomes from virus-driven energy theft and all pathology may never become known. Experimental evidence of biophysically constrained biologically-based cause and effect is not something that most neo-Darwinian theorists have considered. Instead, they report findings that are reported in the science news, like this:
New Scientist, April 23, 2016 High Altitude Survival
Perhaps the most dramatic evidence of modern benefits from ancient DNA is seen in the Tibetans. Emilia Huerta-Sanchez at the University of California in Merced and her colleagues found that about 8 per cent of Tibetans carry a particular piece of Denisovan DNA. Most bits of Denisovan DNA are not present in more than 0.2 per cent of East Asians, so geneticists suspected the ancient DNA must have given its Tibetan owners significant advantages.
The stretch of ancient DNA overlaps with the EPAS1 gene, the Denisovan version of which seems to help people survive the low-oxygen conditions at high elevations. It’s possible that Denisovans were adapted to life at altitude and passed that trait to humans. “But we’ll never know because we cannot take physiological measurements of Denisovans,” says Huerta-Sanchez.
My comment: This news was portrayed by the biologically uniformed David Klousie, in the following context.
A high priority of our aquatic ancestors was to hold their breath longer, those that were able to function in low-oxygen conditions for longer times had a higher probability of providing more food for their children, by being able to access food that was deeper which required holding their breath longer. Seems reasonable to entertain the idea that Denisovans spent a lot of time in the water.
My comment: I am convinced that until RNA methylation is linked to behavior, no one will be forced to admit that their theories have become more ridiculous on almost a daily basis. I look forward to publication of the article that will link RNA methylation to behavior, but wonder how much more nonsense I can tolerate until the end of this month.