YEC compared to Perry Marshall’s opinions

By: James V. Kohl | Published on: March 28, 2016

Heterogeneity in Oct4 and Sox2 Targets Biases Cell Fate in 4-Cell Mouse Embryos
Received: June 9, 2015/ Published: March 24, 2016

In conclusion, we suggest that highly heterogeneous expression of several Oct4 and/or Sox2 targets within the 4-cell embryo, regulated by differential activity of CARM1, creates heterogeneities that bias cell fate toward either an embryonic (pluripotent) or extra-embryonic (differentiating) fate. We further suggest that the highly heterogeneous expression of Sox21 is one of a number of mechanisms available to the embryo to direct cell fate. Our findings that several Oct4 and Sox2 target genes are overrepresented in the subset of highly variable genes at the 4-cell stage and that Sox21 is co-regulated with other transcription factors, such as Nanog and Esrrb, supports this hypothesis. Thus, if a single source of heterogeneity were to be removed, the embryo could compensate for this loss. In summary, our results indicate that heterogeneous gene expression as early as the 4-cell stage initiates cell-fate decisions.

My comment: The ten-month delay follows nearly a 20 year delay in recognition of facts about RNA-mediated cell type differentiation that we included in a section on molecular epigenetics in From Fertilization to Adult Sexual Behavior.  We explained why all aspects of epigenetically-effected RNA-mediated cell type differentiation must be examined in the context of what is known about the links from the immune system to nutrient-dependent sex differences in cell types that have since been extended to all cell type differentiation in all individuals of all living genera.
See also: Design and synthesis of a minimal bacterial genome
Excerpt 1)

…biological functions could not be assigned for the ~31% of the genes that were placed in the generic and unknown classes.

Excerpt 2)

…another major component of living cells is the cell membrane that separates the outer medium from the cytoplasm and governs molecular traffic into and out of the cell. It is an isolatable structure, and many of the syn3.0 genes code for its protein constituents. Because our minimal cell is largely lacking in biosynthesis of amino acids, lipids, nucleotides, and vitamins, it depends on the rich medium to supply almost all of these required small molecules. This necessitates numerous transport systems within the membrane. In addition, the membrane is rich in lipoproteins. Membrane-related genes account for 84 (18%) of the 473 total syn3.0 genes. Included categories from Table 1 are lipoproteins, cofactor transport, efflux systems, protein transport, and other membrane transport systems. Lastly, 81 genes (17%) that are primarily involved in cytosolic metabolism are retained in the categories of nucleotide salvage, lipid salvage and biogenesis, proteolysis, metabolic processes, redox homeostasis, transport and catabolism of nonglucose carbon sources, and glucose transport and glycolysis (Fig. 6).

My comment: If they had read our 1996 review or any of the published works that have since cited it, they might have noticed that the innate immune system is most likely linked to the function biological functions of the ~31% of the genes classified as “generic” and “unknown.”
If they had learned anything about how physics and chemistry must be linked to biophysically constrained nutrient-dependent RNA-mediated protein folding in the context of the physiology of reproduction in all living genera, they might have learned that virus-driven energy theft perturbs cell type differentiation, which is why it is the source of all pathology. Viruses steal the energy that links biophysically constrained cell type differentiation to all biodiversity. That suggests that no one on Venter’s team knows anything more that theorists like Masatoshi Nei, about the structure and function of different cell types.
Masatoshi Nei concluded: 

…genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world. In this view of evolution there is no need of considering teleological elements” (p. 199). Mutation-Driven Evolution

My comment: Why isn’t anyone discussing the link from virus-driven energy theft to mutations and all pathology? Young earth creationists already put the facts about cell type differentiation into their accurate representations of biologically-based cause and effect. Yet, even other Christians are attacking the experimental evidence that links the innate immune system to supercoiled DNA, which protects all organized genomes from virus-driven entropy.
See: Regulatory evolution of innate immunity through co-option of endogenous retroviruses

We speculate that the prevalence of IFN-inducible enhancers in the LTRs of these ancient retroviruses is not coincidental, but may reflect former viral adaptations to exploit immune signaling pathways promoting viral transcription and replication (32).

My comment: I suspect they know how far behind the research they are, and that Greg Bear incorporated what they are speculating into his science fiction novels from 1999 and 2003.
See: The Darwin Code by Greg Bear
See for comparison: Young Earth Creationists killing Christian credibility?
My comment: Perry Marshall is killing his own credibility. Young Earth Creationists reported this:
Viral Genome Junk Is Bunk

Perhaps the evolutionists have placed the cart before the horse on this issue, as proposed by several creationist scientists.4,6 In fact, in an ironic twist, the evidence mentioned above indicates that viruses likely arose from their hosts and not the other way around. As molecular biologist and biochemist Peter Borger notes, “The most parsimonious answer is: the RNA viruses got their genes from their hosts.”6

Ancient virus found hibernating in the human genome—and it might wake up


“Many studies have tried to link these endogenous viral elements to cancer and other diseases, but a major difficulty has been that we haven’t actually found all of them yet,” said co-first author Zachary Williams, also at Tufts.

My comment: There is no need to find all the viruses that cause cancer and all other pathology.  There is a need to understand the fact that cell type differentiation is energy-dependent and that viruses steal that energy. When everyone understands that fact, serious scientists may move forward and focus on prevention and/or effective cures for all virus-caused pathology, i.e., all pathology.

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