The biophysics of metacognition sans mutations

Reported last year in this announcement.  “Metacognition therefore is not restricted to vertebrates and can be accomplished in a much smaller and limited brain.”

In Kohl (2012) “The honeybee is a model organism for understanding the epigenetic link from food odors and social odors to neural networks of the mammalian brain, which ultimately determine human behavior.”

In Kohl (2013) “In the honey bee, the outputs of gene regulatory networks stemming from near identical genomes are altered by differing nutritional intakes which can be considered to be alternate trajectories along an epigenetic landscape. Differential nutrition results in different morphologies, different physiologies, different nervous systems and very different behaviors, all arising from different developmental trajectories that end in queen and worker. (Gabor Miklos & Maleszka, 2011, p. 403)”

In Kohl (2013) “Epigenetics: An essential mechanism for pruning down the wide range of possible behaviors permitted by genes, selecting those that fit an individual’s environment (Berreby, 2011).”

Published Nov 4, 2013 “…nonhuman animals can assess the certainty of a predicted outcome, and bees’ performance was comparable to that of primates in a similar paradigm. We discuss whether these behavioral results prove bees react to uncertainty or whether associative mechanisms can explain such findings. To better frame metacognition as an issue for neurobiological investigation, we propose a neurobiological hypothesis of uncertainty monitoring based on the known circuitry of the honey bee brain.

Feierman, like others: Random mutations are the substrates upon which directional natural selection acts. I’ve frequently asked: “Is there a model for that?” or any experimental evidence in any model organism that supports such a statement?

Published Nov 6, 2013 RNA catalyses nuclear pre-mRNA splicing. “…the common catalytic mechanism used by the spliceosome and group II introns is consistent with a common evolutionary origin between the spliceosome and these ancient RNA retroelements46,47.”

Random mutations that compromise metal binding are not likely to lead to alternative splicings or to natural selection of anything. Mutations typically lead to dead-ends along an evolutionary continuum, which may be why theoretical biologists have begun to disassociate mutations from natural selection.  See: No entailing laws, but enablement in the evolution of the biosphere. Enablement in evolution is something that “just happens” outside the constraints of physics (as in biophysics)

Obviously, there are some people who realize that random mutations are NOT the substrate on which natural selection acts, at the same time others have realized they must eliminate physics and model organisms from consideration of biological facts exemplified in species from microbes to man. We indirectly suggested that random mutations were not involved in the alternative splicings facilitated by RNA catalysis and nuclear pre-mRNA splicing by considering pre-mRNA and alternative splicing in the context of molecular epigenetics in species from microbes to man. In 1996, we wrote: “Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to sexual differentiation in at least two species, Drosophila melanogaster and Caenorhabditis elegans…. That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes.”  I mentioned this in response to a Dec. 2012 article in the Scientist “Evolution by Splicing,” which was based on  two article published in Science Magazine.

Author: James Kohl

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