MicroRNA binds messenger RNA: Adaptive Evolution
‘Junk DNA’ drives embryonic development December 3, 2012 in Genetics
Excerpt: “We now know that microRNAs are far from junk. They… bind messenger RNA, preventing their encoded proteins from being constructed. In this way, microRNAs play important roles in determining which proteins are produced (or not produced) at a given time.
MicroRNAs are increasingly recognized as an important part of both normal cellular function and the development of human disease.”
See: Whole-genome microRNA screening identifies let-7 and mir-18 as regulators of germ layer formation during early embryogenesis. Colas AR, McKeithan WL, Cunningham TJ, Bushway PJ, Garmire LX, Duester G, Subramaniam S, Mercola M. Genes Dev. 2012 Nov 14.
Full text is free here: Conclusion: “Despite major differences in the architecture and developmental strategies that distinguish amphibians and mammals, the interaction between let-7 and Nodal responsiveness define a miR/antagonist–Nodal/agonist module that was selected and evolutionarily conserved in order to shape distinct domains of Nodal activity at this highly dynamic and critical stage of embryogenesis.”
——————————————————————————————————————————————–
The epigenetically effected microRNA /messenger RNA balance is responsible for adaptive evolution of our brain and behavior (in my model).
Kohl (2012) Presented Nov 9. Human Pheromones: Epigenetic Effects of Odors and Their Affects on Behavior
This model of systems biology represents the conservation of bottom-up organization and top-down activation via:
1.Nutrient-dependent stress-induced and social stress-induced intracellular changes in the homeostatic balance of microRNA(miRNA) and messenger RNA (mRNA);
2.Intermolecular changes in DNA (genes);
3.Non-random experience-dependent stochastic variations in de novo gene expression for odor receptors;
4.The required gene-cell-tissue-organ-organ system pathway that links sensory input directly to gene activation in neurosecretory cells of the brain;
5.The required reciprocity that links gene expression to behavior that alters gene expression (i.e., from genes to behavior and back).
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