Counting fish teeth reveals DNA changes behind rapid evolution

Reseachers who make claims about the rapid evolution of teeth in fish but ignore the fact that teeth are ecological adaptations in other organisms must detail the evolutionary event that explains the differences between their claim and my claim that teeth are ecological adaptations, which also are manifested in differences in behavior. They can then try to explain how teeth evolved in fish more rapidly than in nematodes, if that’s what they are claiming.

I am claiming that nutrient-dependent pheromone-controlled de novo Creation of olfactory receptors links changes in morphological and behavioral phenotypes via RNA-mediated amino acid substitutions that stabilize the DNA in organized genomes of species from microbes to man, with teeth and without teeth. For additional information on RNA-mediated changes in the stickleback model organism see: stickleback RNA-mediated,.since my claims have not changed since we first detailed RNA-mediated sex differences in cell types of yeasts, nematodes, and flies in 1996 before turning our attention to cell type differentiation in mammals via the conserved molecular mechanisms in our section on molecular epigenetics.

“Molecular epigenetics. It is now understood that certain genes undergo a process called “genomic or parental imprinting.” Early in embryonic development attached methyl groups become removed from most genes. Several days later, methyl groups are reattached in appropriate sites. Fascinatingly, some such genes reestablish methylation patterns based upon whether the chromosomal segment carrying the gene came from maternal or paternal chromosomes. These sexually dimorphic patterns are labeled genomic or parental imprinting, and these imprintings are inheritable but non-genetic modifications of specific genes (Razin and Shemer, 1995; Reik, 1989; Surani, 1991; Zuccotti and Monk, 1995).

There are at least 16 known genomic-imprintings in the human genome and each particular imprint depends upon whether the chromosome is of maternal or paternal origin (Hurst, McVean, and Moore, 1996). Furthermore, these inherited imprintings are physiologically important and are capable of sex-specific effects as evidenced in the Prader-Willi and Angelman syndromes (congenital disorders with physical and mental characteristics) derived from imprinting anomalies in a specific region of chromosome 15 (Driscoll, Waters, Williams, Zori, Glenn, Avidano, and Nicholls, 1992).

Genomic-imprinting is also manifest in specific parts of the X-inactivation region’s related XIST gene. Here male- and female-specific methyl-group patterns participate in X-inactivation in females and also in the preferential inactivation of the paternal X in human placentae of female concepti (Harrison, 1989; Monk, 1995). This process indicates that tissues of the early conceptus can sense and react differentially to epigenetic sexual dimorphisms on the female conceptus’ own two X chromosomes. Furthermore, variations of X-inactivation patterns often account for traits discordance in monozygotic twin females. In other words, they are often found to have nonidentical patterns of X-inactivation, yielding differing expression of noticeable X-linked traits (Machin, 1996).

Pollard (1996) has hypothesized that sexual orientation may be encoded within imprinted genes. In a manner that also challenges the Gn–H–B paradigm she posits that genomic imprinting, as a preconception event, enables a gene to be “able to switch through different states of potential activity from the incomplete to the fully penetrant state resulting in a continuum of orientations ranging from asexual, through graded bisexual to homosexual” (p. 269). And she envisions these modifications to be potentially prompted by social environmental events.

Yet another kind of epigenetic imprinting occurs in species as diverse as yeast, Drosophila, mice, and humans and is based upon small DNA-binding proteins called “chromo domain” proteins, e.g., polycomb. These proteins affect chromatin structure, often in telomeric regions, and thereby affect transcription and silencing of various genes (Saunders, Chue, Goebl, Craig, Clark, Powers, Eissenberg, Elgin, Rothfield, and Earnshaw, 1993; Singh, Miller, Pearce, Kothary, Burton, Paro, James, and Gaunt, 1991; Trofatter, Long, Murrell, Stotler, Gusella, and Buckler, 1995). 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.

A potential ramification of epigenetic imprinting and alternative splicing may be occurring in Xq28, a chromosomal region implicated in homosexual orientation (Brook, 1993; Hu, Pattatucci, Patterson, Li, Fulker, Cherny, Kruglyak, and Hamer, 1995; Turner, 1995). Xq28 contains one of the X chromosome’s two pseudoautosomal regions (PARs), adjoins the telomere, and has various means of gene expression control (D’Esposito, Ciccodicola, Gianfrancesco, Esposito, Flagiello, Mazzarella, Schiessinger, and D’Urso (1996). Xq28, therefore, is a chromosomal region that has many of the heterochromatic and telomeric characteristics that participate in sexual determination and behavior in other species.”

 

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