Phenotypic plasticity in Astatotilapia burtoni allows individual males to alternate between dominant and subordinate status, two physiologically and behaviorally distinct phenotypes. Because these phenotypes are completely reversible, they provide an excellent model for studying the molecular mechanisms of phenotypic plasticity. The ability to express alternate phenotypes in A. burtoni depends on the ability to regulate gene expression on both short- and long-term time scales. Previous studies have demonstrated that dominant males, who have increased reproductive capacity, have higher expression of several genes involved in reproduction (e.g., genes for steroid receptors). These differences in gene expression and reproductive physiology are controlled by interactions among males. Recently, it was found that the same interactions that lead to stable long-term changes in gene expression also induce short-term and transient changes in expression of egr-1, an immediate-early gene transcription factor. This immediate-early gene response is part of a general mechanism for mediating changes in gene expression that underlie phenotypic plasticity. Longer stable changes in gene expression must involve other mechanisms, such as dynamic modifications of the epigenome. Recent data suggests a direct link between the immediate-early gene response and epigenetic modifications. These mechanisms which link behavioral interactions to changes in gene expression allow phenotypic variation to occur without corresponding changes in the genome and, as a consequence, they have implications for evolution. In the case of A. burtoni, phenotypic plasticity is likely to slow evolution because it produces highly adapted phenotypes under the primary niches encountered in the life-history of the species and the plasticity itself is likely to be an adaptive trait.

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