See first: Natural selection for adaptation (3)

See also: “pericentromeric satellite RNA expression

Did you mean “pericentromeric satellite dna expression

No. I am not a stupid gene-centric theorist. I am a Creationist who knows how energy-dependent supercoiled DNA is Created.

For instance, light-activated microRNA-mediated “Biogenesis is regulated by many checkpoints at every step, primarily at the transcriptional level, in the nucleus, cytoplasm, with RNA regulation, RISC loading, miRNA strand selection, RNA methylation/uridylation, and turnover rate.”

If you have not yet linked God’s Creation of energy-as-information from the pH-dependent physiology of reproduction to biophysically constrained viral latency and all phenotypes, start with Regulation of MicroRNAs 8/26/21.

See also the STEM toy for ages 14+ Genotype.

See for comparison: Evolution and Phylogeny of MicroRNAs – Protocols, Pitfalls, and Problems

An accurate and comprehensive annotation of miRNAs is required as a basis to understand their impact on phenotypic evolution.

If you already know how all energy-dependent biophysically constrained cell type differentiation occurs, refuse to place it back into the context of billions to millions of years of evolve phylogeny. No experimental evidence of biologically-based cause and effect suggests that microRNAs (miRNAs) or phylogeny evolved.

For comparison, all intelligent serious scientists have linked light-activated microRNA biogenesis to healthy longevity and linked the virus-driven degradation of messenger RNA to all diseases.

See: MicroRNAs in Genetic Etiology of Human Diseases

Their roles in cancer, neurodegenerative diseases, and other systemic diseases have been studied broadly. In these regulatory pathways, their mutations and target sequence variations play critical roles to determine their functional repertoire. In this chapter, we summarize studies that investigated the role of mutations, polymorphisms, and other variations of miRNAs in respect to pathological processes.

See also: Role of MicroRNAs in Extreme Animal Survival Strategies 8/26/21

In this chapter, we discuss the activation, expression, biogenesis, and unique attributes of miRNA regulation required to facilitate profound metabolic rate depression and implement stress-specific metabolic adaptations.

Natural selection for stress-specific metabolic adaptations can be compared to stupid theories in which energy emerges and automagically links beneficial mutations from random changes in phenotypes to genotypes via cryptic transcription.

For comparison to ecologically relevant “magic traits,” See: Altered chromatin states drive cryptic transcription in aging mammalian stem cells 8/2/21

…the more permissive chromatin state at intragenic cryptic promoters likely underlies increased cryptic transcription in aged mammalian stem cells.

If you have not linked the virus-driven degradation of messenger RNA to the aging of mammalian stem cells, see: Virus-mediated archaeal hecatomb in the deep seafloor (2016) for comparison to  Eukaryotic plankton diversity in the sunlit ocean (2015).  The conserved molecular mechanisms of diversity across kingdoms have not changed since the beginning of time, and the energy-dependent Peptide synthesis at the origin of life.

If you were tricked into believing anything else by biologically uninformed science idiots, see: Pericentromeric noncoding RNA changes DNA binding of CTCF and inflammatory gene expression in senescence and cancer 8/23/21

Here, it has been revealed that noncoding RNA (ncRNA) transcribed from pericentromeric repetitive elements impairs the DNA binding of CCCTC-binding factor, resulting in the alteration of chromosomal accessibility and the activation of SASP-like inflammatory genes. Notably, the ncRNA was transferred into surrounding cells via small extracellular vesicles, acting as a tumorigenic SASP factor. Our study highlights a novel mechanism regulating chromatin interaction and inflammatory gene expression in senescence and cancer.

Stop letting people who make claims about a novel mechanism attempt to explain away their epic failure to link what is known about the energy-dependent biophysically constrained fixation of RNA-mediated amino acid substitutions and cell type differentiation across kingdoms.

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