番茄SlJAZ7蛋白差异化调控茉莉酸和水杨酸介导的防御反应的分子机理

Signaling crosstalk between jasmonates (JA) and salicylic acid (SA) commonly manifests as a reciprocal antagonism in the plant defense system. Pathogens have evolved to successfully employ this JA-SA antagonistic crosstalk, the mechanism of which has been poorly understood, to suppress plant immune responses and promote disease susceptibility. The bacterial pathogen Pseudomonas syringae pv. tomato DC3000, used as models for understanding plant-bacterial interactions, can secret a polyketide phytotoxin called coronatine (COR), which structurally mimics the plant hormone JA. COR initiates JA signaling through stabilizing the interaction of JAZ repressors with JA-receptor COI1 that results in JAZ degradation, which leads to reduced SA immunity. Our sequence analyses reveal the existence of 13 JAZ proteins (designated as SlJAZ1 to SlJAZ13) in the recently decoded tomato genome. SlJAZ7 is unique among these 13 JAZ proteins. First, SlJAZ7 is most greatly induced by Pst DC3000. Second, due to its unique structural characteristics, SlJAZ7 exhibits significantly reduced degradation rate at the presence of COR compared with Arabidopsis JAZ1 proteins. Third, transgenic plants generated to over-express a JAZ7 full length cDNA (SlJAZ7-OE) exhibit increased resistance to Pst DC3000 infection. These results indicate that SlJAZ7 is evolved to restrict COR-dependent pathogenesis. We further find that SlJAZ7 plays a negative role in regulating JA-dependent plant defense responses, thus a positive role in regulating SA-dependent plant defense responses. Based on the above findings, further exploration of the unique role of SlJAZ7 that differentially regulating JA- and SA-mediated plant defense responses will provide us new insights towards the highly sophisticated defense system plants utilize to restrict Pseudomonas syringae pathogenesis.

茉莉酸和水杨酸在调控植物的防御反应时是相互拮抗的。虽然其分子机理尚不清楚，但病原菌利用了这一特点。丁香假单胞杆菌Pst DC3000可产生活性茉莉酸类似物冠菌素（COR），促进JAZ蛋白的降解，激活茉莉酸途径来拮抗水杨酸途径，实现对植物的侵染。番茄基因组共编码13 个JAZ 蛋白，我们的研究发现SlJAZ7的功能与其它JAZ明显不同：其一，SlJAZ7是番茄JAZ基因家族中受Pst DC3000诱导最强的成员；其二，SlJAZ7具有独特的蛋白结构域，其降解速率明显慢于其它JAZ蛋白；其三， SlJAZ7全长过表达番茄对Pst DC3000抗性显著增强。这暗示SlJAZ7很可能是番茄针对COR进化出来的。进一步研究发现SlJAZ7负向调控茉莉酸途径而正向调控水杨酸途径。以此为基础，我们将研究SlJAZ7差异化调控茉莉酸途径和水杨酸途径的分子机理，并揭示植物利用其对抗丁香假单胞杆菌的调控网络。

茉莉酸和水杨酸在调控植物的防御反应时是相互拮抗的。半寄生型病原菌丁香假单胞杆菌Pst DC3000利用了这一特点，产生活性茉莉酸类似物冠菌素（COR），促进JAZ蛋白的降解，激活茉莉酸途径来拮抗水杨酸途径，实现对植物的侵染。和其他番茄JAZ蛋白不同，过表达JAZ7可显著增强番茄植株对Pst DC3000的抗性，但其分子机理尚不清楚。在本项目中我们揭示了JAZ7差异调控茉莉酸和水杨酸介导的防御反应的分子机理。我们发现JAZ7通过其jas结构域与茉莉酸途径核心转录因子MYC2互作，并抑制MYC2的转录活性，从而负调控茉莉酸介导的防御反应。我们还发现JAZ7可以富集到MYC2靶基因JA2L的启动子区域，间接抑制JA2L对水杨酸代谢基因SAMT1和SAMT2的诱导表达，从而正调控水杨酸介导的防御反应。序列分析表明JAZ7的jas结构域不含有典型的LPIAR基序，而含有LAMAR基序。有趣的是，该基序的差异不影响JAZ7与茉莉酸受体COI1的互作，但使其不易被降解，因此过表达JAZ7可显著增强番茄植株对Pst DC3000的抗性。结合JAZ7是番茄JAZ基因家族中受Pst DC3000诱导最强的成员，我们推测JAZ7很可能是番茄针对COR进化出来的：在受到Pst DC3000侵染后，病原菌释放的COR会快速诱导JAZ7的表达，而JAZ7又不易被降解，因此可以很好地削弱茉莉酸信号途径来增强水杨酸信号途径，实现对丁香假单胞杆菌的有效防御。本研究为系统性了解茉莉酸、水杨酸信号途径及其拮抗关系提供了创新性的知识积累，为打破两种信号途径的拮抗关系提供了基因靶点和思路。