A participant on the ISHE’s yahoo group took a new “out-of-context” approach to the question: “…how [could] random mutations…cause development of eyes…”? (By out-of-context I mean that he uses quotes but does not indicate where the question in the quotes came from, then answers the question as if the context were unimportant.)
On 3/11/13 Sizemore wrote in msg #44875: “…random mutations may be related to phenotypic changes that can then be acted upon by the selective environment. Get it?
My response: No, I don’t “get it.” Is there a model for that? How are the random mutations related to phenotypic changes?
On 3/11/13 Sizemore wrote in msg #44875: “Another way that the genotype and phenotype may change is if the environment changes and begins to exert selection upon existing traits that are tied to genotype.”
My response: In my model of cause and effect, that’s how nutrients epigenetically effect the genotype and how the metabolism of the nutrients to species-specific pheromones enables selection for existing and for novel traits that are tied to genotype.
I think the biological facts have become so obvious that even the most adamant proponents of random mutations theory are being forced to change to an accurate representation of cause and effect.
For example, watch how the moderator of the ISHE group changed his misrepresentations of the role of random mutations from 11/1/12 to 3/13/12.
On 11/1/12 Feierman wrote “Random mutations are the substrates upon which directional natural selection acts.”
On 2/16/13 Feierman wrote: “Random gene mutation is the variance generator upon which natural selection operates.”
On 2/23/13 Feierman wrote in the topic thread with the title Newman 2013 Pigeon Study Contradicts Darwinian Natural Selection: “…random genetic mutations generate the substrate upon which natural selection can act. Random genetic mutations create structural variations in protein enzymes…”
On 3/11/13 in msg #44876 Feierman wrote:
“…random mutation, although the usual substrate for natural selection, is not a sufficient cause of natural selection. Random mutations are a contributing cause. They are not even an essential cause…”
In my model of nutrient-dependent pheromone-controlled thermodynamics and thermoregulation of adaptive evolution, natural selection is for nutrients. The nutrients metabolize to pheromones that control reproduction. Receptor-mediated natural selection for nutrients enables adaptive evolution via pheromone-controlled receptor-mediated ecological, social, neurogenic, and socio-cognitive niche construction.
Now that others, like Feierman, realize random mutations “…are not even an essential cause…” discussion might being about how “…other mechanisms, like immigration or genetic drift, can increase the frequency of new alleles (genes) in a population.”
In my model, new alleles (genes) in a population are nutrient-dependent and pheromone-controlled in species from microbes to man.
See for example: Nutrient-dependent / Pheromone-controlled Adaptive Evolution
and Nutrient-dependent / Pheromone-controlled thermodynamics and thermoregulation
James V. Kohl detailedl how quantized energy-dependent microRNA biogenesis links the pheromone-controlled physiology of reproduction to biophysically constrained viral latency and healthy longevity. Links from what organisms eat to the enzyme-dependent metabolism of food also link metabolic networks to microRNA-mediated genetic networks in the context of RNA interference. Drug therapies alter RNA interference by altering cell type differentiation in all cells of all individuals of all species. For comparison, during the past 26 years, Kohl has detailed how the chemistry of protein folding is biophysically constrained at every level of biological organization by conserved molecular mechanisms.