神经酰胺激酶ACD5在植物程序性细胞死亡和抗病应答中的功能

鞘脂除了作为生物膜的重要组分之外，还作为生物活性分子广泛参与多种生物学过程。acd5 （accelerated cell death5）是自发性死亡突变体，其表型是由鞘脂代谢途径中的重要酶—神经酰胺激酶（ACD5）的突变而引起。研究表明ACD5参与调控植物程序性细胞死亡和抗病性，但其调控的分子机制还不清楚。本申请拟在前期工作的基础上，深入研究1）神经酰胺激酶ACD5在细胞内的时空分布与细胞死亡和抗病性之间的关系；2）ACD5转录调控与蛋白修饰对其功能的影响；3）筛选ACD5互作蛋白，并研究其对ACD5功能的影响；以及筛选4）acd5抑制子。该研究将有助于揭示神经酰胺激酶调控程序性细胞死亡和抗病免疫应答的分子机制，为该蛋白在植物抗病中的有效利用提供理论依据。

Sphingolipids, as essential components of membrane system, are bioactive molecules and participate in many biological processes. Arabidopsis thaliana acd5 mutants that lack ceramide kinase, encoded by ACCELERATED CELL DEATH5 (ACD5), display spontaneous programmed cell death (PCD). The previous study implicates that ACD5 is involved in regulation of cell death control and plant defense responses, however, its molecular mechanisms are still poorly understood. In this study, we will pursue 1) whether temporal and spacial cellular distributions of ACD5 could be regulated in response to cell death and pathogen infection; 2) the impacts of ACD5 transcriptional regulation and protein modification on ACD5 function; 3) screening and verification of the interactive proteins for ACD5; and 4) a suppressor screening for acd5 mutants. This study will help us to uncover the molecular mechanisms how ACD5 contributes to PCD and plant immune responses, and also provides theoretical basis for the effective utilization of ACD5 in plant disease resistance.