Pathogen exploitation of an abscisic acid- and jasmonate-inducible MAPK phosphatase and its interception by Arabidopsis immunity
Pathogen exploitation of an abscisic acid- and jasmonate-inducible MAPK phosphatase and its interception by Arabidopsis immunity
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DOI：
10.1073/pnas.1702613114
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发表时间：
2017-07-11
影响因子：
11.1
通讯作者：
Tsuda, Kenichi
中科院分区：
文献类型：
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作者：
Mine, Akira;Berens, Matthias L.;Tsuda, Kenichi
植物病原体通过例如利用由植物激素如脱落酸（阿坝）和茉莉酸酯（JA）介导的信号传导途径来促进毒力。一些植物可以通过激发一种称为效应子触发免疫（ETI）的有效免疫形式来抵消病原体的毒性。在这里，我们报告阿坝和JA介导的免疫相关的MAP激酶（MAPKs），MPK 3和MPK 6，在拟南芥的失活。阿坝通过ABF/AREB转录因子诱导编码蛋白磷酸酶2C（PP 2Cs）、HAI 1、HAI 2和HAI 3的基因的表达。这三种HAI PP 2C与MPK 3和MPK 6相互作用，并且是ABA介导的MPK 3/MPK 6失活和免疫抑制所需的。细菌病原菌假单胞菌pv.番茄（Pto）DC 3000激活阿坝信号传导并产生一种促进毒力的JAmin模拟植物毒素冠菌素（COR）。我们发现，Pto DC 3000通过COR介导的MYC 2（JA信号传导中的主转录因子）激活诱导HAI 1。HAI 1在体外使MPK 3和MPK 6去磷酸化，并且对于COR介导的MPK 3/MPK 6活化和免疫抑制是必需的。有趣的是，在ETI激活后，A.拟南芥植物通过阻断JA信号转导克服了COR的HAI 1依赖性毒力。最后，我们发现阿坝和JA在其他菊科植物中对HAI PP 2Cs的诱导具有保守性。总之，这些结果表明，阿坝和JA信号通路，这是劫持的细菌病原体，收敛于HAI PP 2C，抑制免疫相关的MAPK的激活。此外，我们的数据揭示了JA信号激活的拦截作为ETI期间针对MAPKs的细菌抑制的宿主对策。
Phytopathogens promote virulence by, for example, exploiting signaling pathways mediated by phytohormones such as abscisic acid (ABA) and jasmonate (JA). Some plants can counteract pathogen virulence by invoking a potent form of immunity called effector-triggered immunity (ETI). Here, we report that ABA and JA mediate inactivation of the immune-associated MAP kinases (MAPKs), MPK3 and MPK6, in Arabidopsis thaliana. ABA induced expression of genes encoding the protein phosphatases 2C (PP2Cs), HAI1, HAI2, and HAI3 through ABF/AREB transcription factors. These three HAI PP2Cs interacted with MPK3 and MPK6 and were required for ABA-mediated MPK3/MPK6 inactivation and immune suppression. The bacterial pathogen Pseudomonas syringae pv. tomato (Pto) DC3000 activates ABA signaling and produces a JAmimicking phytotoxin, coronatine (COR), that promotes virulence. We found that Pto DC3000 induces HAI1 through COR-mediated activation of MYC2, a master transcription factor in JA signaling. HAI1 dephosphorylated MPK3 and MPK6 in vitro and was necessary for COR-mediated suppression of MPK3/MPK6 activation and immunity. Intriguingly, upon ETI activation, A. thaliana plants overcame the HAI1-dependent virulence of COR by blocking JA signaling. Finally, we showed conservation of induction of HAI PP2Cs by ABA and JA in other Brassicaceae species. Taken together, these results suggest that ABA and JA signaling pathways, which are hijacked by the bacterial pathogen, converge on the HAI PP2Cs that suppress activation of the immune-associated MAPKs. Also, our data unveil interception of JA-signaling activation as a host counterstrategy against the bacterial suppression of MAPKs during ETI.