遺伝子と栄養の相互作用における樹状突起形成のメカニズム解明

树突乔木通过在2维（2D）中穿过体壁上皮的内表面生长以及通过从体壁的基底层分离并侵入表皮细胞层而在3D中生长而形成图案。我们发现，通过用含有不同氨基酸水平的食物饲养果蝇幼虫来改变营养状态，会导致树突形状的变化，特别是调节树突侵入下层上皮细胞。我们发现Dystrophin以营养依赖的方式促进树突对上皮细胞的3D侵袭。与此同时，我们监测内源性肌营养不良蛋白的表达，发现肌营养不良蛋白表达在感觉神经元和底层表皮细胞的体壁。总之，我们的数据表明，自闭症谱系障碍的遗传位点中断控制树突图案响应营养状态。

The dendrite arbor is patterned by growing in 2 dimensions (2D) cross the inner surface of the body wall epithelium and in 3D by detaching from the basal lamina of the body wall and invading into the epidermal cell layer. We’ve found that changing nutritional state by raising Drosophila larvae on food containing different amino-acid levels leads to dendritic shape changes and in particular modulating dendrite invasion into underlying epithelial cells. We discovered that Dystrophin promotes the 3D invasions of the epithelial cells by dendrites in a nutrition-dependent manner. In parallel, we monitored endogenous Dystrophin expression and found that Dystrophin was expressed in both sensory neurons and the underlying epidermal cells of the body wall.In summary, our data suggest that a genetic locus disrupted in Autism Spectrum Disorders controls dendrite patterning in response to nutritional state.