Cell type differentiation is included in all topics in biology, which is why it is important to understand what is currently known about top-down causation in the context of physics and chemistry. Taken together, physics, chemistry, and the conserved molecular mechanisms of biology link Drosophila to Octopuses and all other species on this planet via RNA-directed DNA methylation and RNA-mediated amino acid substitutions that differentiate cell types. See for examples: Let there be anti-entropic light (1)
An antagonist led me to ask: “How can anyone who has worked with squid not link light-induced amino acid substitutions in plants and animals to the nutrient-dependent pheromone-controlled physiology of reproduction in bobtail squid via what is currently known about quantum physics, quantum biology, and quantum smell linked to quantum consciousness?”
The ever more antagonistic Ricardo Lara Ramírez responded: “I´ll put it simply: that sentence is at least worth 10 PhD projects together…”
He was berating me for claiming what George F.R. Ellis claimed about top-down causation and what Stuart A. Kauffman claimed about anti-entropy. It’s as if the thought never occurred to him and to several other theoretical physicists that “Life is physics and chemistry and communication” Having no thoughts of their own about top-down causation might explain their attitude towards me. I’ve provided examples of how the anti-entropic epigenetic effects of light and food link physics, chemistry, and communication, to biodiversity.
For another example of how light-induced amino acid substitutions are linked from what organisms eat to their morphological and behavioral phenotypes via the physiology of their nutrient-dependent reproduction see: Honey, I shrunk the ants: How environment controls size and Researchers nearly double the size of worker ants .
These reports address the most recent work that links RNA-directed DNA methylation to RNA-mediated amino acid substitutions and cell type differentiation, which links the physiology of reproduction to the morphological and behavioral phenotypes of species from microbes to man.
The evolution of quantitative traits is therefore thought to occur through random mutations across these loci3,56.
However, the empirical search for QTLs has revealed that trait variation often maps to specific genetic regions of small or large effect, and with specific functions4,57. The apparent gap between the assumptions of the infinitesimal model and the results of QTL analyses is further exacerbated by the fact that countless studies have demonstrated that QTLs cannot in themselves explain all heritable variation underlying quantitative traits5, such as growth or size in humans58, Arabidopsis59 and yeast60.
My comment: We continue to see cell type differentiation accurately portrayed in the context of nutrient-dependent pheromone-controlled fixation of amino acid substitutions in species from yeasts to humans. That links cell type differentiation to light-induced amino acid substitutions in plants. The extension from plants and other animals to modern human populations also has become clear.
Excerpt: The results from a genome-wide, single nucleotide polymorphism (SNP) data strongly support the hybridization model as the best fit for Japanese population history.
My comment: Hybridation is not mutation-driven evolution. Also, in 2014, others reported what appears to be an RNA-mediated UV light-induced amino acid substitution that may be linked from nutrient uptake to RNA-directed DNA methylation and ecological adaptation in a modern human population.
My comment: Nutrient-dependent pheromone-controlled fixation of the replacement of leucine with isoleucine at the 418th amino acid of HYAL2 and suppression of the oncogenic virus Jaagsiekte sheep retrovirus appears to link the viral microRNA / nutrient-dependent microRNA balance and the survival of a modern human population via the physiology of their pheromone-controlled reproduction. There also are similarities in the mouse-to-human model that links EDAR to cell type differentiation from top-down causation to cell type differentiation in the modern Chinese. For example, a single base pair and single amino acid substitution link the mouse model to adaptations in a modern human population in China.
Excerpt: “Two additional recent reports link substitution of the amino acid alanine for the amino acid valine (Grossman et al., 2013) to nutrient-dependent pheromone-controlled adaptive evolution. The alanine substitution for valine does not appear to be under any selection pressure in mice. The cause-and-effect relationship was established in mice by comparing the effects of the alanine, which is under selection pressure in humans, via its substitution for valine in mice (Kamberov et al., 2013).
These two reports (Grossman et al., 2013; Kamberov et al., 2013) tell a new short story of adaptive evolution. The story begins with what was probably a nutrient-dependent variant allele that arose in central China approximately 30,000 years ago.”
My comment: The story is about ecological variation and ecological adaptation that, as usual is told as one about mutations and evolution. But, as we can see in the reports on Epigenetic variation in the Egfr gene generates quantitative variation in a complex trait in ants, it is RNA-directed DNA methylation and RNA-mediated amino acid substitutions that appear to link the epigenetic landscape to the physical landscape of DNA in the organized genomes of all genera.
I will continue to address the fact that their innate ability to respond to viruses and viral microRNAs with nutrient-dependent defenses links metabolic networks and genetic networks to survival and biodiversity, and hope that someone will offer another model of biologically-based cause and effect for comparison — if there is another model.