Results obtained in this study suggest that the number of viruses in deep-sea sediments might be dependent upon complex interactions with both abiotic factors (such as pressure, physical disturbance, and redox conditions) and biotic factors, including bacterial metabolic state and virus supply from the water column. Further studies are needed to clarify the causes of the low viral density, to estimate the actual impact of viruses on benthic microbial functioning, and to assess possible implications for biogeochemical cycles.
Quorum sensing links the physiology of energy-dependent reproduction and virus-driven energy theft from the microRNAome of and light organ of bobtail squid to the bull sperm microbiome, which links microRNAs in breast milk to human brain development. The bacteria that populate the light organ have already been linked by Bonnie Bassler’s group and Margaret McFall-Ngai’s group to everything known about the physiology of energy-dependent reproduction in all living genera.
Anna Di Cosmo’s group and Eugene Daev’s group group may be best prepared to use the information in the context of symbiosis, which links energy-dependent ecological adaptations via olfaction, the innate immune system, microRNA flanking sequences, and supercoiled DNA. The supercoiled DNA links energy-dependent changes from angstroms to ecosystems because it protects all organized genomes from virus-driven energy theft and genomic entropy. Facts that RNA-mediated amino acid substitutions to cell type differentiation will continue to become more important links between the Precision Medicine Initiative and the National Microbiome Initiative
For example, the ratio of bacteria to viruses is a clear indication that ecological adaptation must occur in the bacteria that are hosts to the viruses. If the bacteria did not adapt virus-driven energy theft would have destroyed all ecosystems before there were any ecosytems. That fact suggests ecological variation has always been linked to biodiversity via the energy-dependent innate immune system, which links metabolic networks to genetic networks. So does every other fact known to serious scientists about energy-dependent cell type differentition.
See also:The global ocean microbiome
The ocean microbiome covers the majority of the Earth’s surface, extending an average of more than 2 miles deep to the sea floor. Made up of an extraordinary diversity of microorganisms, the ocean microbiome was one of the first microbiomes to be studied. As its distribution and makeup become better understood, questions about its functional capabilities under stress have grown.
Sunlight or, more specifically, solar UV radiation (UV) acts as the principal natural virucide in the environment. UV radiation kills viruses by chemically modifying their genetic material, DNA and RNA. The most effective wavelength for inactivation, 260 nm (55), falls in the UVC range, so-named to differentiate it from near-UV found in ground-level sunlight, i.e., the UVB and UVA portions of the spectrum, 290 to 320 nm and 320 to 380 nm, respectively (51). Nucleic acids are damaged also by UVB and UVA but with lower efficiency than by UVC radiation (64).
Creationism is difficult to discuss outside the context of energy-dependent creation compared to energy theft and pathology. See for example this attempt at discussion on the “Creationism” FB group.
This open access article may be too technical for most people to discuss, but Creationism is difficult to discuss outside the context of energy-dependent creation compared to energy theft and pathology.
My summary of the excerpt:
They linked energy-dependent changes in base pairs from one SNP and one amino acid substitution to cell type differentiation across populations of modern humans that varies with morphological and behavioral phenotypes.
In the same study they linked virus-driven energy theft to loss of function mutations and transgenerational epigenetic inheritance of healthy longevity for comparison to mutation-driven pathology via the mouse model. The mouse to human model was already used to link the EDAR variant to similar morphological differences in humans. The morphological differences appear to link the Zika virus pathology to craniofacial changes and differences in brain development via what is known about the bull sperm microRNAome and presence of microRNAs in human breast milk that protect infants from virus-driven energy theft during the first few years of development.
The derived G allele at the index SNP in this region (rs3827760) encodes a functional substitution in the intracellular death domain of EDAR (370A) and is associated with reduced chin protrusion (Table 2). EDAR is part of the EDA signalling pathway (comprising EDA, EDAR and EDARADD (the EDAR-binding death domain adaptor protein)) which specifies prenatally the location, size and shape of ectodermal appendages (such as hair follicles, teeth and glands)23. The death domain has been shown to be involved in the interaction of EDAR with EDARADD, the 370A form having higher activity than the ancestral variant24. The G allele at rs3827760 is not present in Europeans and Africans but is seen at high frequency in East Asians and is essentially fixed in Native Americans (Table 3). This SNP has been associated in East Asians with characteristic tooth morphologies, hair type and sweat gland density25, 26, 27. Recently, we showed, in the same study sample examined here, that rs3827760 impacts on aspects of pinna morphology, including: lobe size and attachment, ear protrusion and helix rolling12. Mutations in the EDA pathway cause hypohidrotic ectodermal dysplasia28. This disorder is characterized by a reduced number of sweat glands, oligodontia, decrease in the amount of hair and facial dysmorphia, including a markedly protrusive chin29.”
For ~2 years, the epigenetic effect of light on tissue growth has been reported in the context of DNA repair and none of the biologically uninformed participants here seem to know that light — as energy — is the source of all information required for cell type differentiation and protection from virus-driven energy theft.
See for example: Light coaxes stem cells to repair teeth: Noninvasive laser therapy could radically shift dental treatmenthttps://www.sciencedaily.com/releases/2014/05/140528150559.htm
A Harvard-led team is the first to demonstrate the ability to use low-power light to trigger stem cells inside the body to regenerate tissue.
No one on any of the FB groups I belong to seems to know anything about the anti-entropic epigenetic effects of light. What’s worst is that on the Creationism FB group, Larry Lamb plagiarized our 1996 Hormones and Behavior review and asserted claims about XIST and endogenous retroviruses in the context of cell type differentiation?
“Genomic-imprinting is also manifest in specific parts of the X-inactivation region’s related XIST gene. Here male- and female-specific methyl-group patterns participate in X-inactivation in females and also in the preferential inactivation of the paternal X in human placentae of female concepti (Harrison, 1989; Monk, 1995). This process indicates that tissues of the early conceptus can sense and react differentially to epigenetic sexual dimorphisms on the female conceptus’ own two X chromosomes. Furthermore, variations of X-inactivation patterns often account for traits discordance in monozygotic twin females. In other words, they are often found to have nonidentical patterns of X-inactivation, yielding differing expression of noticeable X-linked traits (Machin, 1996).”
Larry Lamb linked energy-dependent epigenetically-effected cell type differentiation to RNA-mediated events from the advent of sexual differentiation to all cell type differentiation in all individuals of all species that sexually reproduce — from one paragraph of our 1996 review. So did I in subsequent reviews.
But I have since linked the sun’s biological energy to healthy longevity, and linked virus-driven energy theft to all pathology. Larry Lamb added comments about ERVs to her comment (Larry claims to be a she), after several days spent antagonizing me with claims that she did not know what I was talking about. I expect that someday very soon, someone will report the links I have already detailed as if the ideas first occurred to them. If my blog posts seem more scattered across disciplines until then, it’s because I’m trying to cover too much that’s in the news.
Yesterday, for example, this report of research on alternative splicings of pre-mRNA was published as: Rare evolutionary event detected in the lab
See also from From Fertilization to Adult Sexual Behavior
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.
I don’t care who gets the credit for revealing the links from sunlight to RNA-mediated cell type differentiation. But I am disgusted by reports that place everything known about the energy dependent de novo creation of biogeochemical systems, which includes the the innate immune system, into the context of evolutionary events.
See for example: Spliceosomal intronogenesis
They do not know how the spliceosomal introns emerged, or why only eukaryotes possess this class of introns. But they claim “…it is widely accepted that the spliceosomal introns originated from the group II self-splicing introns and appeared at the time of eukaryogenesis (11, 18).”
My comment: What is not known is widely accepted as the origins of introns that automagically appeared at the time of eukaryogenesis.
They claim that proto-spliceosomal introns resembled the group II introns and link them across some period during which “…they retained their mobility and self-splicing ability (5).”
My comment: Now we have the unknown origins of introns with self-splicing ability.
The automagical emergence of the self-splicing ability may have enabled and promoted proliferation of the introns until the group II intron-derived features automagically degenerated over time. The magic of evolution then lead to a necessity for the development of the pre-mRNA splicing machinery, which was automagically composed of trans-acting snRNAs and trans-acting protein factors. That’s how they arrived at their conclusion that “…reverse splicing-catalyzed intron transposition is an appealing model for intron gain.”
Caveat: For an intron gain event to become fixed in a population in the context of evolution, the intron insertion must result in a selective advantage in the context of an ecological niche and speciation. They claim there may be means other than reverse splicing that could be highly mosaic among individuals. Thus, they conclude there may be “…multiple mechanisms of intron gain that may change over time and genetic circumstance.”
That is what was reported as the Rare evolutionary event detected in the lab.
In other words, anything that happens to any organism can be placed into the context of rare evolutionary events that lead to change over time depending on genetic circumstances.