Evolution of Intelligent Viruses and Jumping Genes
Conclusion: “…it is intelligent warfare between mobile genetic elements and the epigenetic responses of the cell that, most likely, determines evolution.”
My comment: This conclusion appears to place biologically-based cause and effect into the context of viruses and evolved immune system responses. Epigenetically-effected immune system responses can be compared in the context of epigenetic effects on cell type differentiation that link ecological variation to ecological adaptation.
This puts cause and effect into their proper perspective. Ecological variation leads from top-down causation to epigenetic effects. The epigenetic effects appear to involve microRNAs that change the microRNA/messenger RNA balance, which lead to RNA-mediated differences in cell types via chromatin remodeling. That places cell type differentiation into the context of Jon Lieff’s 2012 claim that “…alternative splicing may be the critical source of evolutionary changes differentiating primates and humans from other creatures such as worms and flies with a similar number of genes.” That claim can be compared to the conclusion reached in the 2013 textbook Mutation-Driven Evolution “…genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world (p. 199).” Our section on molecular epigenetics in our 1996 Hormones and Behavior review can also be compared to claims that anything except RNA-mediated events lead to the increasing complexity of biodiversity.
First, however, the role of viruses must be placed into the context of ecological variation and cell type differentiation via chromatin remodeling and RNA-mediated amino acid substitutions. See for example:
The pig as a large animal model for characterization of host-pathogen interactions
Excerpt: “…we were able to perform highly controlled experimental infections and to study changes of symptoms, viral titer, and expression of microRNAs/mRNAs as the influenza infection progressed in time…”
My comment: They linked the immune system response to viruses and cell type difference in the host across the course of the infection.
Excerpt: The fact that EBV and the closely related rLCV both encode sequence-related pre-miRNAs that give rise to two different miRNAs with the same functionality, implies that these pre-miRNAs diverged from a common ancestor that also shared these atypical features.
Reported as: Study reveals how a cancer-causing virus blocks human immune response
My comment: That news report and the two articles link amino acid substitutions in viruses to cell type differentiation in all cells of all individuals of all species via conserved molecular mechanisms. Amino acid substitutions appear to differentiate some, if not all, viruses. See for examples:
Excerpt: When we introduced aspartic acid-to-alanine substitution at position 97 (D97A) of the resistant virus carrying glutamine at position 120 to disrupt hydrogen bond formation, the resultant virus became moderately sensitive.
2) Biological and Structural Characterization of a Host-Adapting Amino Acid in Influenza Virus
Excerpt 1) “…a basic amino acid at position 591 of PB2 can compensate for the lack of lysine at position 627 and confers efficient viral replication to pandemic H1N1 viruses in mammals.”
Excerpt 2) “These differences may affect the protein’s interaction with viral and/or cellular factors, and hence its ability to support virus replication in mammals.”
My comment: Amino acid substitutions in viruses are linked to amino acid substitutions that differentiate the cell type of species from microbes to man. See for review: Kohl (2013)
A single amino acid substitution differentiates the cell types of common strains of Escherichia coli and the Escherichia coli (EHEC) serotype O157:H7 that is responsible for outbreaks of bloody diarrhea. ” “D-serine influences both gene content and regulation of critical virulence factors in pathogenic E. coli.”
The next step required to link the epigenetic landscape to the physical landscape of DNA requires links from quantum physics to quantum biology via the chemistry of RNA-mediated protein folding.
Quantum dot/antibody conjugates for in vivo cytometric imaging in mice was reported earlier today as Quantum dots combined with antibodies as a method for studying cells in their native environment
I will follow-up on this with a post that links the sun’s biological energy to cell type differentiation.
