Burmeister Sabrina S
Department of Biology, University of North Carolina, Chapel Hill, NC 27599-3280, USA.
Brain Behav Evol. 2007;70(4):247-56. doi: 10.1159/000105488. Epub 2007 Sep 18.
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.
布氏非鲫的表型可塑性使个体雄性能够在优势和从属两种生理和行为上截然不同的表型之间转换。由于这些表型是完全可逆的,它们为研究表型可塑性的分子机制提供了一个绝佳的模型。布氏非鲫表达交替表型的能力取决于在短期和长期时间尺度上调节基因表达的能力。先前的研究表明,具有增强繁殖能力的优势雄性,其几个参与繁殖的基因(如类固醇受体基因)表达较高。这些基因表达和生殖生理的差异是由雄性之间的相互作用控制的。最近发现,导致基因表达稳定长期变化的相同相互作用,也会诱导早期即刻基因转录因子egr-1表达的短期和瞬时变化。这种早期即刻基因反应是介导作为表型可塑性基础的基因表达变化的一般机制的一部分。基因表达中更长时间的稳定变化必须涉及其他机制,如表观基因组的动态修饰。最近的数据表明早期即刻基因反应与表观遗传修饰之间存在直接联系。这些将行为相互作用与基因表达变化联系起来的机制,使得表型变异能够在基因组无相应变化的情况下发生,因此,它们对进化具有影响。就布氏非鲫而言,表型可塑性可能会减缓进化,因为它在该物种生活史中遇到的主要生态位下产生高度适应的表型,而且可塑性本身可能是一种适应性特征。