Cell lineage tracing in the developing enteric nervous system: superstars revealed by experiment and simulation
Excerpt: “The experiments and model suggest that stochastic competition for resources is an important concept when understanding biological processes which feature high levels of cell proliferation. The results have implications for cell-fate processes in the ENS.”
My comment: The results have implications for cell-fate processes in every cell of every organism of every species. Stochastic competition for resources is the model I detailed in: Nutrient-dependent/pheromone-controlled adaptive evolution: a model, which was based on other published works, including Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors.
In the context of stochastic competition for resources, and linking the enteric and central nervous systems, I wrote:
Excerpt: Just as the influence of diet and pheromones can be in the larval stages or in other developmental stages of insects, it can also be in the pre- and postconception stages of mammals, including humans (Fowden et al., 2006; Mennella, Jagnow, & Beauchamp, 2001). For example, pheromones and nutrition could alter levels of maternal hormones, gestational events, and postnatal outcomes via their direct effect on maternal GnRH and the placenta. The outcomes might not always be positive, which means the possible effects should not be ignored. That would be like ignoring the likely effects of docosahexaenoic acid in the maternal and postnatal diet on LH and on neuronal development in the mammalian brain (Lassek & Gaulin, 2011).
Excerpt from (Lassek & Gaulin, 2011). “This suggests that increasing dietary intake of n-3 and decreasing n-6 fatty acids may have cognitive benefits in children, especially in females.”
My comment: Watch for the important role of fatty acids like docosahexaenoic acid to be noticed more than 2 years later when it’s reported below in: Monkeys that eat omega-3 rich diet show more developed brain networks based on Dietary Omega-3 Fatty Acids Modulate Large-Scale Systems Organization in the Rhesus Macaque Brain [subscription required]
The ability to link ecological variation, such as variation in fatty acid intake, to the enteric nervous system and to the central nervous system is crucial to any accurate representation of biologically-based cause and effect in birds (vertebrates) or bees (invertebrates). Nutrient-dependent pheromone-controlled adaptations link ecological variation to the enteric nervous system and to the central nervous system in all organisms with ecologically adapted enteric nervous systems and central nervous systems.
The fact that the link only shows up in organisms with digestive systems and nervous systems should not be used to dismiss the connection from self vs non-self identification in microbes via genetically predisposed differences in cell types of organisms, because differences in cell types exist in the same species.
Recent experiments show that cells, which were once thought to be the same cell type, have subtle differences in their metabolism. That means evolutionary theorists should stop telling peoples that mutation-driven evolution is exemplified in experiments like those reported by Richard Lenski’s group. His experiments continue to lead to misrepresentations of biologically based cause and effect that are widely reported.
From the time of their first replication, it is clearly that innate genetically predisposed differences in the cell metabolism of one cell differentiates it from other cells. Looking downstream after 50,000 generations leads to the wrong conclusion. It shows how an immeasurably subtle difference in the thermodynamics of intracellular signaling lead to differences in organism-level thermoregulation attibuted to mutation-driven antibiotic resistance and mutation-driven evolution.
Besides, there is no model of conserved molecular mechanisms that suggests mutation-driven evolution is possible. There are only models of population genetics, such as those incorporated into Lenski’s experiments. Those mathematical models dismiss the fact that mutations perturb the stability of protein folding, which is required for speciation via ecological adaptations.
That’s why Lenski’s results are reported in terms of theory. He frames the results in the context of mutation-driven evolution because people believe that mutations cause evolution. Mutations perturb protein folding, which is why they may cause diseases and disorders. Biophysical constraints on ecological adaptations ensure that protein folding is not perturbed so that species diversity is ensured in species from microbes to man.
The straightforward proposal of mutation-driven evolution is accepted in the context of “evolution for dummies” but it has been accepted by so many dummies that it continues to be more difficult to separated the dummies from the serious scientists who have learned about the conserved molecular mechanisms of ecological adaptations. In reports that include what is known about the conserved molecular mechanisms of ecological adaptations we read things like this: “At the RNA level, each cell in what was thought to be a rather homogeneous population shows differential expression of transcripts across the genome [2-4]. Indeed, at a recent meeting, one presenter studying a gene whose allelic forms show strong quantitative expression variation at the RNA level (eQTL) in cell populations concluded that genetics don’t determine expression at the individual cell level. This was the interpretation of the data even though summing expression from each allele over many individual cells gave the same biased distribution of expression as seen using bulk populations… ” Mutations in genes cannot initiate natural selection because receptor proteins link the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man. Mutations that perturb the folding of receptor proteins do not link anything to anything else. When deleterious mutations accumulate in the DNA, they lead to a intracellular dead end, or to an organism dead end. Mutations are not beneficial and cannot be naturally selected.
Nutrients are be naturally selected. As promised, above, see for example: Monkeys that eat omega-3 rich diet show more developed brain networks
Article excerpt 1): The study measured a kind of omega-3 fatty acid called docosahexaenoic acid, or DHA, which is a primary component of the human brain and important in development of the brain.
My comment: The article clearly links ecological variation in the availability of DHA to differences in cell types of the human brain, which are the result of nutrient-dependent pheromone-controlled adaptations. The adaptations are manifested in Mosaic Copy Number Variation in Human Neurons.
Article excerpt 2): “The data shows the benefits in how the monkeys’ brains organize over their lifetime if in the setting of a diet high in omega-3 fatty acids,” said Damien Fair, PA-C, Ph.D., assistant professor of behavioral neuroscience and assistant professor of psychiatry in the OHSU School of Medicine and senior author on the paper. “The data also shows in detail how similar the networks in a monkey brain are to networks in a human brain, but only in the context of a diet rich in omega-3-fatty acids.”
My comment: The data do not show that monkeys somehow mutated into humans, and Lenski’s data do not show that E. coli mutates into some other species of bacteria. No data shows that because it is not possible given what is already known about the biophysical constraints on nutrient-dependent pheromone-controlled protein folding in species from microbes to man.
The question arises: Is someone like PZ Myers teaching your kids to be dummies?