No experimental evidence of biophysically constrained biologically-based cause and effect supports claims that the mammalian placenta “evolved.”
All experimental evidence of biophysically constrained biologically-based cause and effect supports claims that the mammalian placenta is an energy-dependent pheromone-controlled ecological adaptation.
Chemoautotrophic symbiosis is nutrient energy-dependent and pheromone-controlled. Nothing about life involves autotrophy. Everything known to serious scientists links chirality to autophagy, which protects the supercoiled DNA of all organized genomes from virus-driven energy theft and genomic entropy that links extinction to the fossil record. Claims about the last known common ancestor of shipworms are the clearest indicator that pseudoscientists do not realize no last known common ancestor has ever been found for any form of energy-dependent RNA-mediated life.
“We made history!” marchers chanted at the terminus of a mile-and-a-half walk from the Washington Monument to Capitol Hill in Washington, DC.
“We just watched a documentary on Charles Darwin the other night, and my older daughter, when I told her that in some countries—Turkey, Russia, and parts of the United States—evolutionary theory is taken out of the school curricula, she said, ‘We have to make a sign!’ And we [created] these ones.” —Percy Rohde
“I’ve never done this and I am so excited to be here.” —Peggy Mikros, caterer from Chicago
Here’s a sampling of sights and signs from the Marches for Science in Berlin, Chicago, and Washington, DC.
Here is the scientific support for what my sign would have said;
The ARID1A gene, encoding a subunit of the ATP-dependent chromatin remodeling complex SNF/SWI, has recently been identified as a tumor suppressor in multiple cancers. Despite studies that elucidate the mechanism of ARID1A’s tumor suppressor function, little is known of the genes/events that regulate ARID1A expression. Using the HEK293 cells as a model, we discovered novel aspects of ARID1A transcription regulation in response to cell cycle progression, DNA damage, and microRNAs, exemplifying the potential of our strategy in providing new insight to the mechanism of gene transcription regulation.
I don’t know any serious scientist who has ever started with a claim about evolution, mutation, or natural selection. All serious scientists know they must start with the energy-dependent de novo creation of ATP, and link it to cell type differentiation in all living genera via the physiology of pheromone-controlled reproduction.
See for a historical perspective: Dependence of RNA synthesis in isolated thymus nuclei on glycolysis, oxidative carbohydrate catabolism and a type of “oxidative phosphorylation” (1964)
The synthesis of RNA in isolated thymus nuclei is ATP dependent.
Connecting energy as information to ATP-dependent synthesis of RNA and healthy longevity is not difficult unless you do not know where the energy comes from. If you do not know or fail to acknowledge the creation of energy as the source that links the anti-entropic virucidal effects of sunlight to all biodiversity via what is known to serious scientists, you will not understand what serious scientists know about how to prevent all virus-driven energy theft from linking mutations to all pathology in all living genera
The architecture of chromatin is governed, in part, by adenosine triphosphate (ATP)-dependent chromatin remodelers. These multi-protein complexes contain targeting domains that recognize posttranslational marks on histones. One such targeting domain is the bromodomain (BD), which recognizes acetyl-lysines and recruits proteins to sites of acetylation across the genome. Polybromo1 (PBRM1), a subunit of the polybromo-associated BRG1- or hBRM-associated factors (P-BAF) chromatin remodeler, contains six tandem BDs and is frequently mutated in Renal Clear Cell Carcinoma (ccRCC). Mutations in the PBRM1 gene often lead to loss of protein expression; however, missense mutations in PBRM1 have been identified and tend to cluster in the BDs, particularly BD2 and BD4, suggesting that individual BDs are critical for PBRM1 function. To study the role of these six BDs, we inactivated each of the six BDs of PBRM1 and re-expressed these mutants in Caki2 cells (ccRCC cells with loss of function mutation of PBRM1). Four of the six BDs abrogated PBRM1 tumor suppressor, gene regulation, and chromatin affinity with degree of importance correlating strongly to rate of missense mutations in patients. Furthermore, we identified BD2 as the most critical for PBRM1 and confirmed BD2 mediated association to histone H3 peptides acetylated at lysine 14 (H3K14Ac), validating the importance of this specific acetylation mark for PBRM1 binding. From these data we conclude that four of the BDs act together to target PBRM1 to sites on chromatin; when a single BD is mutated, PBRM1 no longer controls gene expression properly, leading to increased cell proliferation.
Yet another kind of epigenetic imprinting occurs in species as diverse as yeast, Drosophila, mice, and humans and is based upon small DNA-binding proteins called “chromo domain” proteins, e.g., polycomb. These proteins affect chromatin structure, often in telomeric regions, and thereby affect transcription and silencing of various genes (Saunders, Chue, Goebl, Craig, Clark, Powers, Eissenberg, Elgin, Rothfield, and Earnshaw, 1993; Singh, Miller, Pearce, Kothary, Burton, Paro, James, and Gaunt, 1991; Trofatter, Long, Murrell, Stotler, Gusella, and Buckler, 1995). 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.
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The American population developed, during thousands of years, free of epidemics that had been attacking Europe, Asia and Africa. The European and African migrations, after Columbus’s first trip, produced an epidemic invasion of influenza, smallpox, measles, yellow fever, malaria, diphtheria, typhus, and other diseases that attacked the immunologically virgin populations and produced a very high mortality, with a diminution of the indigenous population of more than 90% in many places. According to historical evidence, the first epidemic was influenza, produced by swine strain of virus, immediately followed by smallpox. The Spaniards mated freely with the Indians producing a mixed race called the Mestizo, who were immunologically more capable of defending themselves against various viruses, bacteria, and parasites brought over from the Old World. Marriage between the races also was sanctioned by Queen Isabella (1503) and Fernando I (1515). With these new genetic immunologic defenses against infections, the Mestizo eventually made up the majority of the population of Indians in the New World.
Viruses are the most abundant biological entities in the world’s oceans, and they play a crucial role in global biogeochemical cycles. In deep-sea ecosystems, archaea and bacteria drive major nutrient cycles, and viruses are largely responsible for their mortality, thereby exerting important controls on microbial dynamics. However, the relative impact of viruses on archaea compared to bacteria is unknown, limiting our understanding of the factors controlling the functioning of marine systems at a global scale. We evaluate the selectivity of viral infections by using several independent approaches, including an innovative molecular method based on the quantification of archaeal versus bacterial genes released by viral lysis. We provide evidence that, in all oceanic surface sediments (from 1000- to 10,000-m water depth), the impact of viral infection is higher on archaea than on bacteria. We also found that, within deep-sea benthic archaea, the impact of viruses was mainly directed at members of specific clades of Marine Group I Thaumarchaeota. Although archaea represent, on average, ~12% of the total cell abundance in the top 50 cm of sediment, virus-induced lysis of archaea accounts for up to one-third of the total microbial biomass killed, resulting in the release of ~0.3 to 0.5 gigatons of carbon per year globally. Our results indicate that viral infection represents a key mechanism controlling the turnover of archaea in surface deep-sea sediments. We conclude that interactions between archaea and their viruses might play a profound, previously underestimated role in the functioning of deep-sea ecosystems and in global biogeochemical cycles.