由Sclerotinia sclerotiorum引起的菌核病是我国油菜第一大病害，但是该病害抗性资源匮乏，抗性分子机制研究也还不够深入，尤其在油菜作物本身的研究更少。侵染早期活性氧迸发积累是植物对包括S. sclerotiorum在内的多种病原物抗性的重要机制。但目前对该活性氧迸发的转录调控机制尚不明确。本项目拟在油菜上研究Ca2+信号途径重要转录因子CAMTA3对活性氧积累以及菌核病抗性的调控功能，明确油菜CAMTA3调控活性氧积累的结构-功能关系，鉴定油菜CAMTA3转录调控靶标基因以及互作蛋白，阐明油菜CAMTA3转录调控活性氧积累和菌核病抗性的分子机制。所获结果将揭示活性氧和菌核病抗性调控新机制，有力促进对活性氧这个植物抗病性关键因子的分子调控机制的认识，同时增进对菌核病抗性分子机制的理解，并为菌核病抗性新种质创制和抗病新品种分子选育提供基因资源。

The white mould disease caused by Sclerotinia sclerotiorum, is the most devastating disease in oilseed rape. Resistance resource for this disease is lacking, and molecular mechanisms underlying the resistance to this disease are poorly understood. Such kind of research in rapeseed is especially lacking. Oxidative burst is an important mechanism of plant resistance to many pathogens including S. sclerotiorum. However, the transcriptional regulating mechanism underlying the oxidative burst is currently unclear. This project aims to analyze the functions of CAMTA3, an important transcription factor of calcium signaling, in regulating accumulation of reactive oxygen species (ROS) and resistance to Sclerotinia white mould disease in oilseed rape, dissect the structure-function relationship in regulating ROS accumulation, identify new target genes for transcriptional regulation and interacting proteins of BnCAMTA3, thereby elucidate the molecular mechanisms of BnCAMTA3 to regulate ROS accumulation and S. sclerotiorum resistance. The achieved results should unveil a new mechanism for ROS and resistance to S. sclerotiorum, and thus provide insights into the molecular mechanisms of regulation of ROS accumulation, the key factor to initiate disease resistance, as well as improve the molecular mechanisms of regulation of resistance to white mould disease. Meanwhile, this project could provide a set of resistance regulatory genes that are potentially usefull for breeding of improved resistance to white mould disease.