细胞程序性死亡（PCD）是最重要的生物学过程之一，也是植物抗病的重要机制。植物进化了复杂的分子网络来精细地调控PCD，其中的分子机制还有待于进一步解析。类病斑突变体在没有病原物侵染的条件下启动PCD，是解析植物PCD调控机理的钥匙。莽草酸途径是植物最重要的代谢通路之一，但它与PCD的关系还知之甚少。在前期研究中我们发现了一个短日照依赖的类病斑突变体lis1，其突变基因编码莽草酸途径的关键酶；通过遗传筛选我们获得了至少20个lis1突变体的抑制子。本项目将在此基础上结合遗传学、转录组学、代谢组学、生物化学与分子生物学等手段研究LIS1调控植物PCD的机理。本研究将有助于揭示莽草酸途径和PCD的关系、鉴定调控PCD的新基因、发现调控PCD的新机制、为提高植物的抗病性提供新线索，具有重要的科学意义和潜在的应用价值。

Programmed Cell Death（PCD）is not only one of the most important biological processes, but also an important mechanism of disease resistance in plants. Plants have evolved complex molecular network to sophisticatedly regulate PCD, and the underlying molecular mechanisms remain to be further elucidated. Lesion mimic mutant initiates PCD in the absence of pathogen infection and is the key to decipher how plants regulate the PCD. Shikimic acid pathway is one of the most important metabolic pathways in plants. However，the relationship between shikimic acid pathway and PCD is not well-studied. Previously, we identified a short-day-dependent lesion mimic mutant lis1, in which the key enzyme involved in shikimic acid pathway is mutated. Through genetic screen, at least 20 suppressors of lis1 have been isolated. In this proposal, we will further study how LIS1 regulates PCD using integrated approaches of genetics, transcriptomics, metabolomics, biochemistry and molecular biology. This study will help to uncover the relationship between shikimic acid pathway and PCD, to identify new PCD genes, to reveal new PCD mechanisms, and to provide new insights into disease resistance in plants. Therefore, this study is of both scientific significance and potential application value.