Science 30 November 2012: Vol. 338 no. 6111 p. 1125 This Week in Science
“Many mammals have imprinted alleles, where the paternal or maternal version is solely expressed during reproduction. In humans, one such imprinted gene set is the growth promoter insulin-like growth factor 2 (IGF2) and its binding inhibitor, IGF2R mannose 6-phosphate/IGF2 receptor. To avoid parental conflict in fetal growth, imprinting regulates expression of these genes so that expression of IGF2R in the fetus quenches IGF2 and prevents fetus overgrowth through high-affinity binding of IGF2 to IGF2R. Williams et al. (p. 1209) demonstrate that high-affinity binding of IGF2 to IGF2R is present in placental and marsupial mammals; absent in birds and fish; and present, with a 10-fold lower affinity, in monotreme (egg-laying) mammals. The appearance of exonic splicing enhancers in exon 34 of the IGF2R of monotremes appears to have been a key mutational event leading to the establishment of higher affinity, which may have been driven by selection to minimize parental conflict.”
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My comment: The note above describes a key mutational event that appears to involve a ligand-receptor gene set. When a set of genes evolves for better glucose utilization through imprinting, which requires reciprocity as does maintenance of the microRNA / messenger RNA balance required for homeostatsis, is it still appropriate to explain the adaptation via mutation theory?
In my model of adaptive evolution for glucose uptake in mammals, which starts with yeast cells at the advent of sexual reproduction, the difference in receptor-mediated nutrient chemical uptake is expressed via the metabolism of nutrient chemicals to a species-specific ‘sex’ pheromone. Sex pheromones and other pheromones control reproduction in species from microbes to man via nutrient chemical-dependent pheromone-controlled ligand-receptor binding and receptor-mediated behavior.
Invertebrate juvenile hormone is conserved, and gonadotropin releasing hormone (GnRH) is the conserved vertebrate ligand (across 400 million years of adaptive evolution). Diversification of the GnRH receptor is linked to nutrient chemical-dependent speciation in vertebrates via the epigenetic effects of olfactory/pheromonal input and the evolved ability for better glucose utilization. Adaptations for glucose utilization support ecological, social, neurogenic, and socio-cognitive niche construction via epigenetic effects on behavior.
I do not know if another model details how mutations cause adaptive evolution, but suspect there is no other model for the required reciprocity that transgenerationally links gene expression to behavior and back via the epigenetic effects of nutrient chemicals and pheromones, which are exemplified in the honeybee model organism. This brings up the question: Should the term “mutation” be redefined in the context of nutrient chemical-dependent pheromone-controlled adaptive evolution via transgenerational epigenetic inheritance? The article by Williams et al., [Subscription required] suggests to me it should be.
For example, the authors write on page 1212: “The evolution of splicing is underpinned by a complicated multifactorial network of molecular interactions, which cannot be expected to reduce to a single factor (20).” If the evolution of splicing is not reduced to a single factor, how can adaptive evolution be reduced to a series of single mutations? How could a single mutation or series of mutations control the nutrient chemical-dependent behavior unless it was concurrently paired with a mutation or mutations in one or more pheromone receptors?
If ever two concurrent mutations are required, they are much less likely to randomly occur. But that’s another story, and it’s a story that is frequently told by evolutionary theorists. The theorists, perhaps without realizing it, argue that the 4.5 million interactive DNA switches in the human genome evolved via random mutations. For contrast, I think others have learned about levels of biological complexity that could only have evolved if every nutrient ever ingested by any organism contributed to its ability to survive and reproduce via nutrient chemical metabolism to pheromones that control reproduction and adaptive evolution in species from microbes to man.
That story can now be told in the context of Williams et al (2012) who report on 2 of the ~80 genes imprinted in mammals. I first learned of parental imprinting when ~ 16 known genomic-imprintings in the human genome were known to cause an imprint that depended on whether the chromosome was of maternal or paternal origin. Whether 2 of the ~80 or ~16 of the ~80 are involved in epigenetic effects on intracellular signaling and stochastic gene expression that link the adaptive evolution of microbes to man via olfaction and odor receptors as in my model, we can now be rather certain that genomic imprinting for glucose utilization occurs in species from microbes to man.
