Reservoir of mutations enabled cichlid fish to adapt to varied environments
Excerpt: “…the East African cichlid genomes possess an excess of gene duplications; alterations in regulatory, nonprotein-coding elements in the genome; accelerated evolution of protein-coding elements, especially in genes for pigmentation; and other distinct features that affect gene expression, such as insertions of transposable elements and regulation by novel microRNAs.”
My comment: The gene duplications are nutrient-dependent, which means they are biophysically constrained. That fact links ecological variation in the availability of nutrients to biophysically-constrained changes in the microRNA/messenger RNA balance via seemingly futile cycles of thermodynamically-controlled protein biosynthesis and degradation.
Nutrients typically stabilize the DNA in organized genomes via odor-induced de novo Creation of invertebrate and vertebrate olfactory receptor genes. The de novo Creation of receptors enables receptor-mediated behaviors that begin when cells acquire more of the nutrients that stabilize organism-level thermoregulation via amino acid substitutions, which differentiate all cell types of all individuals of all species.
Cell type differentiation via amino acid substitutions is manifested in the morphological and behavioral phenotypes of species from microbes to man via the conserved molecular mechanisms we detailed in our 1996 Hormones and Behavior review article.
“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 (Adler and Hajduk, 1994; de Bono, Zarkower, and Hodgkin, 1995; Ge, Zuo, and Manley, 1991; Green, 1991; Parkhurst and Meneely, 1994; Wilkins, 1995; Wolfner, 1988). That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes.”
Sex differences in cell types link nutrient uptake to the pheromone-controlled physiology of reproduction. In the most recent misrepresentation of biologically-based cause and effect in cichlid fish, different groups of researchers collectively report that mutations cause biodiversity that is clearly nutrient-dependent and pheromone-controlled via conserved molecular mechanisms in species from microbes to man. The mutations are linked to natural selection in the context of population genetics.
Excerpt: “Cichlid phenotypic diversity encompasses variation in behaviour, body shape, coloration and ecological specialization. The frequent occurrence of convergent evolution of similar ecotypes (Fig. 1) suggests a primary role of natural selection in shaping cichlid phenotypic diversity10, 11.”
My comment: They suggest mutations and natural selection somehow lead to morphological and behavioral phenotypes that exemplify nutrient-dependent pheromone-controlled ecological, social, neurogenic, and socio-cognitive niche construction in the context of increasing organismal complexity. That complexity requires the de novo Creation of proteins via nutrient-dependent amino acid substitutions.
Therefore, it is important to note that Jordan et al., (2005) clarified this fact. “We cannot conceive of a global external factor that could cause, during this time, parallel evolution of amino acid compositions of proteins in 15 diverse taxa that represent all three domains of life and span a wide range of lifestyles and environments. Thus, currently, the most plausible hypothesis is that we are observing a universal, intrinsic trend that emerged before the last universal common ancestor of all extant organisms.”
The authors of The genomic substrate for adaptive radiation in African cichlid fish collectively ignore that fact. They attempt to link the evolution of cichlids to their last universal common ancestor via mutations and natural selection. They also continue to ignore the role of nutrient-dependent changes in the microRNA/messenger RNA balance in cell type differentiation via amino acid substitutions as if that level of ignorance was acceptable to serious scientists.
This forces me to repeat Dobzhansky’s (1964) claim: “…the only worthwhile biology is molecular biology. All else is “bird watching” or “butterfly collecting.” Bird watching and butterfly collecting are occupations manifestly unworthy of serious scientists!”
Fifty years later, watching cichlids diversify (e.g., supposedly during the past 15,000 to 100,000 years) and attributing their adaptive radiation to mutations and natural selection is akin to bird watching and butterfly collecting more than 40 years after Dobzhansky noticed that “…the so-called alpha chains of hemoglobin have identical sequences of amino acids in man and the chimpanzee, but they differ in a single amino acid (out of 141) in the gorilla.”
I am reminded that others attributed human evolution to mutations despite clear examples in the mouse-to-human model of nutrient-dependent receptor-medicated amino acid substitutions and pheromone-controlled ecological adaptations manifested in differences in hair, teeth, skin, and mammary tissue. Differences in the behavior of fish and other vertebrates can be addressed in the same context. For example, see MicroRNA-Driven Developmental Remodeling in the Brain Distinguishes Humans from Other Primates: “These results support a scenario, where tissue-specific changes in the expression of trans-regulators, such as miRNA, rather than sequence changes in cis-regulatory regions, are the driving force underlying developmental remodeling across hundreds of genes.”
A recent report on the molecular epigenetics of Fragile X Syndrome, links a mutation to a disorder, not to adaptation and radiation. Clearly, serious scientists must learn to recognize the difference between how nutrient-dependent changes to the microRNA/messenger RNA balance link the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man, so that the changes can be compared to what happens in the context of mutations.