MicroRNAs have been shown to be involved in a wide range of biological processes such as cell cycle control, apoptosis and several developmental and physiological processes including stem cell differentiation, hematopoiesis, hypoxia, cardiac and skeletal muscle development, neurogenesis, insulin secretion, cholesterol metabolism, aging, immune responses and viral replication. In addition, highly tissue-specific expression and distinct temporal expression patterns during embryogenesis suggest that microRNAs play a key role in the differentiation and maintenance of tissue identity.
My comment: The link to viral replication may be the most important aspect of what is currently known about microRNAs. Viral microRNAs appear to link entropic elasticity to cell cycle control by nutrient-dependent microRNAs. That explains why thermodynamic cycles of protein synthesis and degradation can be linked from the anti-entropic epigenetic effects of nutrient-dependent microRNAs to RNA-mediated cell type differentiation. For example, nutrient-dependent RNA-directed DNA methylation and RNA-mediated amino acid substitutions stabilize the biophysically constrained chemistry of protein folding. That’s how difference in protein folding are linked to proper epigenetically-effected DNA organization during the life history transitions of all organisms.
This was reported by Science Mission as: Proper DNA organization is required for cell’s normal functioning
Chromatin, the structure composed of DNA and proteins that makes up chromosomes. Its main role is to package DNA molecules containing all the organism’s genes into the cell nucleus, which is approximately 20,000 times smaller than the DNA itself.
Chromatin is carefully organized in such a way that genes remain “accessible” to the various proteins required for gene expression, or the interpretation of the genic information stored in DNA.Chromatin therefore provides the organism with another layer of information, referred to as epigenetic information, which is made available, in part, through specialized histones called histone variants.This extreme compaction is made possible by proteins called histones, which condense the DNA much like thread is wound around a spool. Authors studied one histone variant called H2A.Z. H2A.Z is located in specific regions of the gene called promoters, which are involved in controlling gene expression. It is known that H2A.Z is necessary for promoters to function properly.”With this study, we discovered that two other proteins (FACT and Spt6) play an important role in the location of H2A.Z,” adds Dr. Jeronimo. “In fact, we found that these proteins are essential to prevent an accumulation of H2A.Z in inappropriate regions of the gene, which leads to a disorganized chromatin structure.”The study also reveals that inhibiting the inappropriate positioning of H2A.Z is crucial to prevent gene expression defects called “cryptic transcription”.Inappropriate H2A.Z localization has previously been observed in cancer cells, but little was understood about the consequences of this phenomenon and this study suggests that mislocalization of H2A.Z may lead to cryptic transcription in some types of cancer such as lymphoma, and this may contribute to the disease.
For more information about how microRNAs are linked from RNA-mediated amino acid substitutions to proper DNA organization in species from microbes to humans, see:
Spag17 encodes a protein present in cilia and flagella with a “9+2” axoneme structure. SPAG17 protein is present in the central pair complex (CPC). It is the orthologue of Chlamydomonas reinhardtii PF6 , a protein located on a projection from the C1 CPC microtubule in green algae . Domains near the C-terminus of PF6 are essential for flagellar motility and assembly of the C1a projection.
My comment: Spag17 encodes a protein that links the light-induced de novo creation of amino acids to RNA-mediated amino acid substitutions that differentiate the cell types of all individuals of all genera via the conserved molecular mechanisms of biophysically constrained nutrient-dependent protein folding in species from microbes to humans. What this research showed was that claims about the re-evolution of the bacterial flagellum in 4 days can be placed into the context of how ecological variation is linked to nutrient-dependent ecological adaptations via the physiology of reproduction.
The only way for the structure and function of the flagellum to arise is in the context of nutrient-dependent RNA-mediated fixation of amino acid substitutions in the proteins needed to construct a functional “propeller-type” mechanism of overwhelming complexity. After disabling the molecular mechanisms that first led to the creation of the flagellum, researchers showed that it quickly reappeared. When it reappeared after only 4 days they still claimed that mutations had caused it to re-evolve. However, everything known to serious scientists about microRNAs and RNA-mediated cell type differentiation shows that functional structures do not arise in the context of mutations and evolution in any organism.
Functional structures are nutrient-dependent because amino acids are required for the formation of proteins in the functional structures. The amino acids that are required to form and maintain the functional structures are fixed in the organized genomes of all genera via their physiology of reproduction. In species from microbes to humans, the physiology of reproduction is nutrient-dependent and pheromone-controlled. Ecological variation in the number and types of viruses links viral microRNAs to genomic entropy, except when nutrient-dependent microRNAs prevent virus-driven entropic elasticity from becoming genomic entropy. The nutrient-dependent microRNAs enable the DNA organization that is required for cell’s normal functioning.
In the broader sense, our work suggests that the chromatin signature of promoters depends not only on specific deposition at promoters but also on selective reincorporation during transcription. Therefore, the promoter signature is intimately linked to the state of chromatin at distal sites. Although this was demonstrated here for the histone variant H2A.Z, the phenomenon may also apply to other chromatin/epigenetic marks.
Although our observations were made in budding yeast, several reasons suggest that our findings translate into higher eukaryotes, including humans.
My comment: Those reasons include the fact that RNA-directed cell type differentiation is biophysically constrained by the nutrient-dependent chemistry of RNA-mediated amino acid substitutions in species from microbes to humans. See for review, our section on molecular epigenetics in:
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.
See also: Perspective / Structural Biology
Theories about mutations and evolution have failed to link what is known about the anti-entropic epigenetic effects of the sun’s biological energy to control of viral microRNA damage by nutrients and fixation of amino acid substitutions in the context of the physiology of reproduction. Those ridiculous theories can now be compared to facts linked to the structural biology that is the basis for Photosystem I (PSI), which “…is an extremely efficient solar energy converter, producing one electron for nearly every photon absorbed (1).”
My comment: If you think that this photosystem could somehow have emerged from nothing, and after constructing itself, could also maintain itself for billions of years, your thoughts could be compared to the results reported as:
“It seems astounding that life has not evolved for more than 2 billion years—nearly half the history of the Earth,” said J. William Schopf, a UCLA professor of earth, planetary and space sciences in the UCLA College who was the study’s lead author. “Given that evolution is a fact, this lack of evolution needs to be explained.”
My comment: The claim that “evolution is a fact” needs to be explained. All experimental evidence links ecological variation to ecological adaptations via the biophysically constrained chemistry of nutrient-dependent RNA-mediated amino acid substitutions and protein folding. Claims that evolutionary forces are involved must be substantiated by experimental evidence that shows why anything other than ecological variation need be linked to ecological adaptations. There may be no more need for claims about evolution because they have been replaced by what is known about ecological adaptations.
This evolutionary scenario is much more complex than is typically envisioned by evolutionary models. Nevertheless, these cyanobacterial communities are ultimately subject to the same laws of population genetics as other systems. Rosen et al. show that with appropriate theoretical and experimental methods, it is possible to characterize the evolutionary forces acting in these cyanobacteria. The authors do so with much less raw sequencing data than would be required in the case of single-cell genomics. Their approach shows how carefully designed empirical methods, guided by theoretical expectations, make it possible to tease apart the ecological and evolutionary forces that shape complex patterns of diversity in microbial communities.
My comment: Ecological forces establish the links between biologically-based cause and effect. Evolutionary forces were invented based on de Vries definition of “mutation” and the assumptions of population geneticists who decided how long it might take for accumulated mutations to cause one species to evolve into another. If not in 2 billion years in some bacteria or 4 days in the other bacteria that reconstructed their flagella, how long do you think it will take for theorists to evolve common sense?
See for review: Fine-scale diversity and extensive recombination in a quasisexual bacterial population occupying a broad niche
My comment: They seem to think others should be motivated to study microbial diversity in the context of epigenetic effects of light gradients, bacteriophages, atmospheric gases, and migration of localized populations. Greg Bear thought that, too. Nearly twenty years ago. See: The Darwin Code: Intelligent Design without God
In 1996, I proposed to my publishers a novel about the coming changes in biology and evolutionary theory. The novel would describe an evolutionary event happening in real-time–the formation of a new sub-species of human being. What I needed, I thought, was some analog to what happens in bacteria. And so I would have to invent ancient viruses lying dormant in our genome, suddenly reactivated to ferry genes and genetic instructions between humans.
To my surprise, I quickly discovered I did not have to invent anything. Human endogenous retroviruses are real…
My comment: What is currently known to serious scientists about viral microRNAs and genomic entropy suggests that without the sun’s biological energy, which links the de novo creation of amino acids to nutrient-dependent microRNAs and RNA-mediated amino acid substitutions, our planet could not sustain life. It certainly could not “evolve” it, or link mutations that perturb protein folding to biodiversity. I’m not sure what Greg Bear meant with inclusion of Intelligent Design without God in the title (above). Perhaps he meant to imply that intelligent design without God would be a waste of time. The viruses would have led to the extinction of all life. That’s not too intelligent a design, is it? Compared to the de novo creation of amino acids that stabilize organized genomes in all genera, intelligent design is like Nature without Nurture.