PROTEIN INTERACTIONS REGULATING MECHANOSENSATION

这项工作的长期目标是阐明分子 线虫的机械感觉基础。身份识别 控制线虫触觉机械感受器的基因 细胞还将用于定义神经退化所需的元素 因为特定的触摸相关突变可以诱导神经元溶解。 蛋白质内假定功能结构域的直接缺失分析 参与退变将被执行，并将促进后续 旨在分离编码与蛋白质相互作用的基因的研究 这些结构域来调节神经元的反应。替代方法 涉及机械感觉调节器的遗传筛选和 用酵母菌两种方法检测体内蛋白质-蛋白质相互作用 提出了杂交系统来识别新的调控基因和 描述现有基因之间的相互作用。其含义是 这项工作在于这些线虫基因可能会提供 对人类神经细胞死亡机制的洞察。此外，基于 在与哺乳动物的同源性上，这些基因中的几个似乎 对离子通道的组件进行编码。因此，这些研究也是相关的。 有助于我们理解与离子运输相关的紊乱。

The long-term objectives of this work are to elucidate the molecular basis of mechanosensation in the nematode C. elegans. The identification of genes which regulate the mechanosensory apparatus in C. elegans touch cells will also serve to define elements required for neurodegeneration since specific touch-related mutations can induce neuronal lysis. Deletion analysis of putative functional domains within proteins directly involved in degeneration will be performed and will facilitate subsequent studies designed to isolate genes encoding proteins that interact with these domains to regulate neuronal responses. Alternative approaches involving genetic screens for modulators of mechanosensation and detection of protein-protein interactions in vivo, using the yeast two- hybrid system are proposed to identify novel regulatory genes and characterize interactions between existing genes. The implications of this work lie in the possibility that these nematode genes will provide insights into mechanisms of human nerve cell death. Additionally, based on homology to mammalian counterparts, several of these genes appear to encode components of ion channels. Thus, these studies are also relevant to our understanding of disorders related to ion transport.