RIPK和RBOHD调控缓慢持续型活性氧迸发的分子机制

活性氧迸发是非常重要的植物免疫反应之一，主要由NADPH氧化酶RBOHD产生，但RBOHD是如何调控活性氧迸发的时空特异性还仍然未知。细菌外膜的脂多糖作为一个典型的微生物相关分子模式（MAMPs），诱导拟南芥产生双相活性氧迸发，早期与其它MAMPs相似，但后期与效应因子诱导的活性氧迸发更相似，表现为缓慢持续型活性氧迸发动态，目前对于这种缓慢持续型活性氧迸发的分子机理还知之甚少。我们前期遗传学研究发现胞内类受体激酶RIPK是脂多糖诱导双相活性氧迸发所必须的，同时也在效应因子诱导的缓慢持续型活性氧迸发中起作用，因此本申请拟进一步研究RIPK和RBOHD调控脂多糖诱导拟南芥双相活性氧迸发的分子机理，通过与效应因子诱导的活性氧迸发对比，阐明缓慢持续型活性氧迸发的共同机制和生物学意义，最后在番茄中验证SlRIPK调控缓慢持续型活性氧迸发分子机理的普遍性和保守性，为植物广谱抗病性育种提供理论指导。

The production of reactive oxygen species (ROS) is a conserved immune response and primarily mediated by a NADPH oxidase, also known as respiratory burst oxidase homologs D (RBOHD) in plants. However, how RBOHD regulated the temporal and spatial specificity of ROS production is still unclear. Lipopolysaccharides (LPS), a typical bacterial MAMP, triggered a biphasic ROS burst, in which the first ROS burst was similar to that induced by other microbe-associated molecular patterns (MAMPs), and the second ROS burst showed a slow and prolonged kinetics which was similar to the effector-triggered ROS burst. The molecular mechanisms underlying the slow and prolonged ROS burst are still poorly understood. In our preliminary data, we performed a genetic screen for Arabidopsis mutants that showed no ROS burst after the LPS treatment, and one was mutated in RIPK (RPM1-Induced Protein Kinase), encoding a cytosolic receptor-like kinase. RIPK was not only required for LPS-triggered biphasic ROS burst, but also MAMP- and effector-triggered ROS burst. Therefore, in this application, we proposed to further decipher the molecular mechanisms of LPS-induced biphasic ROS burst mediated by RIPK and RBOHD, especially the slow and prolonged ROS burst. We will confirm the function of RIPK in the production of slow and prolonged ROS in tomato. Taken together, we believe that our studies about the regulation of ROS will provide a strategy to engineer broad-spectrum disease resistance in crop plants in future.