Epigenetic maintenance of transcription / neuronal migration

By: James V. Kohl | Published on: January 13, 2013

Science 11 January 2013: Vol. 339 no. 6116 pp. 204-207 DOI:10.1126/science.1229326
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Ezh2 Orchestrates Topographic Migration and Connectivity of Mouse Precerebellar Neurons

Excerpt: “During brain development, epigenetic mechanisms allow tangentially migrating neurons to retain topographical organization.”
Article Extract: “Here, we addressed the role of Ezh2, which is member of the Polycomb repressive complex 2 and trimethylates histone H3 at lysine 27 (H3K27me3) (9).”
My comment:
In our 1996 Hormones and Behavior review, (Diamond, Binstock, Kohl) we addressed “chromo domain” proteins, e.g., polycomb in the context of gonadotropin releasing hormone neuronal migration and prenatal sexual differentiation in mammals. The section head is:
“Molecular epigenetics” 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.”
I have since taken our model further to include nutrient chemical-dependent (e.g., glucose) epigenetic effects in placental mammals that are modulated by social stressors via the epigenetic effects of pheromones. I hope the authors here will reply and address migration in the context of ecological, social, neurogenic, and socio-cognitive niche construction. I think what they’ve just shown us exemplifies the molecular biology of epigenetically driven adaptive evolution. Doesn’t it?

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