Summary: 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
My comment: Viruses are not life forms. They steal the quantized energy that links sunlight to viral latency in the context of everything known to all serious scientists about the fact that Feedback loops link odor and pheromone signaling with reproduction
See for comparison: Olfaction Warps Visual Time Perception Energy as information links the sense of smell in bacteria to our visual perception of energy and mass in the context of the space-time continuum and food odors that link the physiology of reproduction in bacteria to the pheromone-controlled physiology of reproduction and biophysically constrained viral latency in all living genera.
…the I662N substitution in mammalian Dnmt3b conferred enhanced chromatin DNA methylation activity and contributed to functional adaptation in the epigenetic system.
Energy-dependent amino acid substitutions link what organisms eat to their pheromone-controlled physiology of reproduction and chromosomal rearrangements that have been linked to all biodiversity via the sense of smell in bacteria and quorum sensing.
An environmental drive evolved from that of nutrient ingestion in unicellular organisms to that of pheromone-controlled socialization in insects. In mammals, food odors and pheromones cause changes in hormones such as LH, which has developmental affects on pheromone-controlled sexual behavior in nutrient-dependent reproductively fit individuals across species of vertebrates.
There are at least four sources of R mutations in normal cells: quantum effects on base pairing (30), mistakes made by polymerases (31), hydrolytic deamination of bases (32), and damage by endogenously produced reactive oxygen species or other metabolites (33).
…their covalently bonded 13C/15N nuclei were assigned using heteronuclear single/multiple quantum coherence correlation experiments (HSQC or HMQC).
…/the observed extremely fast decoherence should be viewed as general, bringing to question any significant quantum coherent transport contributions to photosynthesis.
My summary: Two researches in NATURE denied the role that microRNAs play epithelial-mesenchymal transition in tumors and their denial of everything known about food energy-dependent biophysically constrained pheromone-contolled biodiversity is discussed in this review. See for comparison the section on Regulation of miRNA on EMT in tumors
The role of miRNA/ZEB in head and neck squamous cell carcinoma, in breast cancer, in lung cancer, in pancreatic cancer and in bladder cancer was anticipated in reports by serious scientists such as the late Eshel Ben-Jacob. See: MicroRNA-based regulation of epithelial–hybrid–mesenchymal fate determination, which was reported as:
They found that there is a molecular “on” and “off” switch that cancer cells use to determine their fate. Evidently, there is an on or off state for metastasis (migration), but also a third possibility, according to this recently-discovered molecular data.
The researchers discovered that there was an intermediate function, which is termed a “ternary,” or three-way switch. This function relates to the fact that ZEB has the ability to turn itself on due to a positive feedback system. This allows a cell to keep intermediate levels of all four proteins required for the switch. Ben-Jacob notes that the hybrid, or partially on-off state, also supports cancer metastasis by enabling collective cell migration and by imparting stem-cell properties that help migrating cancer cells evade the immune system and anticancer therapies.
Our results suggest that partial EMT, i.e. a hybrid E/M phenotype, need not be ‘metastable’, and strengthen the emerging notion that partial EMT, but not necessarily a complete EMT, is associated with aggressive tumor progression.
The food energy-dependent stability of the hybrid epithelial/mesenchymal phenotype has been linked from photosynthesis to the creation of energy-dependent microRNAs in plants and in animals via what has been known to all serious scientists about the physiology of pheromone-controlled reproduction in bacteria.
2009 Learning from Bacteria about Natural Information Processing with my emphasis
Focusing on the energy, matter, and thermodynamic imbalances provided by the environment, Schrodinger proposed that life required the consumption of negative entropy, that is, the use of thermodynamic imbalances in the environment. From the perspective of thermodynamics, each bacterium can be viewed as a complex system that is composed of an “engine” that uses imbalances in the environment to do work, and a “machine” that uses this energy (to act against the natural course of entropy increase) for the synthesis of organic substances.13 A third information-processing system is also needed for the coordination and synchronization of the functioning of the engine and the machine. Namely, a living cell is analogous to a complex man-made cybernetic system, or a “chimera,” composed of information processing systems and of at least two thermodynamic elements. In addition, using the outer membrane, cells sense the environment.
We proposed that, besides “negative entropy,” organisms sense the environment to extract latent embedded information.13 By latent information we refer to data embedded in the environment that, once processed cognitively, initiates change in the organism’s function or behavior. Information induces changes; hence it can be used to generate an internal condensed description (model or usable information) of the environment, which guides the organism’s functioning.
Conclusion: Olfaction Warps Visual Time Perception Energy as information links the sense of smell in bacteria to our visual perception of energy and mass in the context of the space-time continuum and food odors that link the physiology of reproduction in bacteria to the pheromone-controlled physiology of reproduction in all living genera.
See for comparison (Koonin is a co-author): On the Origin of Reverse Transcriptase-Using CRISPR-Cas Systems and Their Hyperdiverse, Enigmatic Spacer Repertoires
…another cause of the lack of detectable protospacers is likely to be the existence of a virtually untapped pool of mobile genetic elements that, at any given time, are not represented in a given environment (10). This paucity of spacer matches is conceivably explained by the vastness and diversity of viromes…
Biologically uninformed evolutionary theorists have failed to link the anti-entropic virucidal energy of the sun to all biodiversity and failed to link the virus-driven degradation of messenger RNA to all pathology via changes in the microRNA/messenger RNA balance. The release of the game “Cytosis” in September (2017) will make all theorists appear to be among the biologically uninformed science idiots who invented ridiculous theories in attempts to explain away Darwin’s “conditions of life.”
A board game taking place inside a human cell! Players compete to build enzymes, hormones and receptors and fend off attacking Viruses!
See also the comments on: Stem cell divisions, somatic mutations, cancer etiology, and cancer prevention
Cancer etiology: assumptions lead to erroneous conclusion
The authors claim that cancer is caused and driven by mutations, and that two-thirds of the mutations required for cancer are caused by unavoidable errors arising during DNA replication. The first claim is based on the somatic mutation theory. The second claim is based on a highly positive correlation between the lifetime number of stem cell divisions in a tissue and the risk of cancer in that tissue, and on their method for estimating the proportion of mutations that result from heredity (H mutations), environmental factors (E mutations) and unavoidable errors arising during DNA replication (R mutations). These claims raise several questions:
1. Sequencing studies have found zero mutations in the genes of a variable proportion of different cancer types (see, e.g., https://dx.doi.org/10.1093/jnci/dju405 and references therein). If cancer is caused by mutations in driver genes, could the authors explain what causes these cancers with zero mutations? Could the authors use their method for estimating the proportion of cancer risk that is preventable and unpreventable in people with tumors lacking driver gene mutations?
2. Environmental factors are known to affect stem cell division rates. According to IARC, drinking very hot beverages probably causes esophageal cancer (Group 2A). If you drink something hot enough to severely damage the cells lining the esophagus, the stem cells located in deeper layers have to divide to produce new cells to replace the damaged cells. These stem cell divisions, triggered by an environmental factor, will lead to mutations arising during DNA replication. However, these mutations are avoidable if you do not drink very hot beverages. Should these mutations be counted as environmental mutations (H mutations) or as unavoidable mutations arising during DNA replication (R mutations)?
3. The authors’ work is based on the somatic mutation theory. This theory is primarily supported by the idea that cancer incidence increases exponentially with age. Since our cells are known to accumulate mutations throughout life, the accumulation of driver gene mutations in our cells would perfectly explain why the risk of cancer increases until death. However, it is now well established that cancer incidence does not increase exponentially with age for some cancers (acute lymphoblastic leukemia, testicular cancer, cervical cancer, Hodgkin lymphoma, thyroid cancer, bone cancer, etc). It is also well known that cancer incidence decreases late in life for many cancer types (lung cancer, breast cancer, prostate cancer, etc). For example, according to SEER cancer statistics review, 1975-2014, men in their 80s have approximately half the risk of developing prostate cancer than men in their 70s. The somatic mutation theory, which is the basis for this article, does not explain why the lifetime accumulation of driver gene mutations in the cells of many tissues is not translated into an increase in cancer incidence throughout life. Are the authors’ conclusions applicable to all cancers or only to those few cancers in which incidence increases exponentially with age until death?
4. The authors estimate that 23% of the mutations required for the development of pancreatic cancer are associated with environmental and hereditary factors; the rest (77%) are mutations arising during DNA replication. However, Notta et al. recently found that 65.4% of pancreatic tumors develop catastrophic mitotic events that lead to mutations associated with massive genomic rearrangements (https://doi.org/10.1038/nature19823). In other words, Notta et al. demonstrate that cell division not only leads to mutations arising during DNA replication, but also to mutations arising during mitosis. For this cancer type, the authors could introduce a fourth source of mutations, and estimate the proportion of mutations arising during mitosis (M mutations) and re-estimate those arising during DNA replication (R mutations). Alternatively, they could reanalyze their raw data without assuming that the parameters “stem cell divisions” and ”DNA replication mutations” are interchangeable. Cell division, process by which a cell copies and separates its cellular components to finally split into two cells, can lead to mutations occurring during DNA replication, but also to other cancer-promoting errors, such as chromosome aberrations arising during mitosis, errors in the distribution of cell-fate determinants between the daughter cells, and failures to restore physical interactions with other tissue components. Would the authors’ conclusions stand without assuming that the parameters “stem cell divisions” and ”DNA replication mutations” are interchangeable?
5. The authors report a striking correlation between the number of stem cell divisions in a tissue and the risk of cancer in that tissue. They do not report any correlation between the number of mutations in a tissue and the risk of cancer in that tissue; in fact, these parameters are not correlated (see. e.g., https://doi.org/10.1038/nature19768). In addition, the authors discuss that most of the mutations required for cancer are a consequence, not a cause, of the division of stem cells. So, why do the authors use their correlation to say that cancer is caused by the accumulation of mutations in driver genes instead of saying that cancer is caused by the accumulation of cell divisions in stem cells?
For references and additional information see: Comment on ‘Stem cell divisions, somatic mutations, cancer etiology, and cancer prevention’ DOI: 10.13140/RG.2.2.28889.21602 https://www.researchgate.net/publication/318744904; also https://www.preprints.org/manuscript/201707.0074/v1/download
See also: Miguel Lopez-Lazaro
My comment: Like him, others from a new generation of researchers, will no longer tolerate the pseudoscienitfic nonsense touted by evolutionary theorists and “Big Bang” cosmologists who know nothing about natural selection for energy-dependent codon optimality, which links the physiology of reproduction to biophysically constrained viral latency.