Hou Yuxuan, Wang Yifeng, Tang Liqun, Tong Xiaohong, Wang Ling, Liu Lianmeng, Huang Shiwen, Zhang Jian
State Key Lab of Rice Biology, China National Rice Research Institute, Hangzhou 311400, China.
State Key Lab of Rice Biology, China National Rice Research Institute, Hangzhou 311400, China.
iScience. 2019 Jun 28;16:499-510. doi: 10.1016/j.isci.2019.06.009. Epub 2019 Jun 11.
Bacterial blight caused by the infection of Xanthomonas oryzae pv. oryzae (Xoo) is a devastating disease that severely challenges the yield of rice. Here, we report the identification of a "SAPK10-WRKY72-AOS1" module, through which Xoo infection stimulates the suppression of jasmonic acid (JA) biosynthesis to cause Xoo susceptibility. WRKY72 directly binds to the W-box in the promoter of JA biosynthesis gene AOS1 and represses its transcription by inducing DNA hypermethylation on the target site, which finally led to lower endogenous JA level and higher Xoo susceptibility. Abscisic acid (ABA)-inducible SnRK2-type kinase SAPK10 phosphorylates WRKY72 at Thr 129. The SAPK10-mediated phosphorylation impairs the DNA-binding ability of WRKY72 and releases its suppression on AOS1 and JA biosynthesis. Our work highlights a module of how pathogen stimuli lead to plant susceptibility, as well as a potential pathway for ABA-JA interplay with post-translational modification and epigenetic regulation mechanism involved.
由水稻白叶枯病菌（Xanthomonas oryzae pv. oryzae，简称Xoo）感染引起的白叶枯病是一种毁灭性病害，严重威胁着水稻产量。在此，我们报告了一个“SAPK10-WRKY72-AOS1”模块的鉴定结果，Xoo感染通过该模块刺激茉莉酸（JA）生物合成的抑制，从而导致对Xoo的易感性。WRKY72直接结合JA生物合成基因AOS1启动子中的W-box，并通过诱导靶位点的DNA高甲基化来抑制其转录，最终导致内源JA水平降低和对Xoo的易感性增加。脱落酸（ABA）诱导的SnRK2型激酶SAPK10在第129位苏氨酸处使WRKY72磷酸化。SAPK10介导的磷酸化损害了WRKY72的DNA结合能力，并解除了其对AOS1和JA生物合成的抑制。我们的工作揭示了一个病原体刺激如何导致植物易感性的模块，以及一条涉及翻译后修饰和表观遗传调控机制的ABA-JA相互作用的潜在途径。
