Differential Phosphorylation of the Transcription Factor WRKY33 by the Protein Kinases CPK5/CPK6 and MPK3/MPK6 Cooperatively Regulates Camalexin Biosynthesis in Arabidopsis
Differential Phosphorylation of the Transcription Factor WRKY33 by the Protein Kinases CPK5/CPK6 and MPK3/MPK6 Cooperatively Regulates Camalexin Biosynthesis in Arabidopsis
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蛋白激酶 CPK5/CPK6 和 MPK3/MPK6 转录因子 WRKY33 的差异磷酸化协同调节拟南芥中 Camalexin 的生物合成
DOI：
10.1105/tpc.19.00971
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发表时间：
2020-05
期刊：
影响因子：
11.6
通讯作者：
Meng Xiangzong
中科院分区：
文献类型：
--
作者：
Zhou Jinggeng;Wang Xiaoyang;He Yunxia;Sang Tian;Wang Pengcheng;Dai Shaojun;Zhang Shuqun;Meng Xiangzong
病原体响应性蛋白激酶CPK 5/CPK 6和MPK 3/MPK 6通过转录因子WRKY 33的差异磷酸化协同调节病原体感染后的camalexin生物合成。Camalexin是一种重要的植物抗毒素，在拟南芥（Arabidopsis thaliana）的抗病性中起着重要作用。我们以前的特点是调控camalexin生物合成的丝裂原活化蛋白激酶MPK 3和MPK 6及其下游转录因子WRKY 33。在这里，我们报告说，病原体响应钙依赖蛋白激酶5（CPK 5）和CPK 6也调节拟南芥camalexin生物合成。化学诱导的组成型活性CPK 5或CPK 6变体的表达足以诱导转基因拟南芥植物中的camalexin生物合成。因此，CPK 5和CPK 6的同时突变损害了由真菌病原体灰葡萄孢（Botrytis cinerea）诱导的拟南芥中camalexin的产生。此外，我们鉴定了WRKY 33在CPK 5/CPK 6下游起作用以激活Camalexin生物合成基因，从而诱导Camalexin生物合成。CPK 5和CPK 6与WRKY 33相互作用并磷酸化其Thr-229残基，导致WRKY 33的DNA结合能力增加。相比之下，MPK 3/MPK 6介导的WRKY 33在其N-末端Ser残基上的磷酸化增强了WRKY 33的反式激活活性。此外，获得和丧失功能的遗传分析都证明了CPK 5/CPK 6和MPK 3/MPK 6对Camalexin生物合成的协同调节。综上所述，这些发现表明WRKY 33作为CPK 5/CPK 6和MPK 3/MPK 6的会聚底物发挥作用，CPK 5/CPK 6和MPK 3/MPK 6通过WRKY 33活性的差异磷酸调节协同调节camalexin生物合成。
The pathogen-responsive protein kinases CPK5/CPK6 and MPK3/MPK6 cooperatively regulate camalexin biosynthesis upon pathogen infection via differential phosphorylation of the transcription factor WRKY33. Camalexin is a major phytoalexin that plays a crucial role in disease resistance in Arabidopsis (Arabidopsis thaliana). We previously characterized the regulation of camalexin biosynthesis by the mitogen-activated protein kinases MPK3 and MPK6 and their downstream transcription factor WRKY33. Here, we report that the pathogen-responsive CALCIUM-DEPENDENT PROTEIN KINASE5 (CPK5) and CPK6 also regulate camalexin biosynthesis in Arabidopsis. Chemically induced expression of constitutively active CPK5 or CPK6 variants was sufficient to induce camalexin biosynthesis in transgenic Arabidopsis plants. Consistently, the simultaneous mutation of CPK5 and CPK6 compromised camalexin production in Arabidopsis induced by the fungal pathogen Botrytis cinerea. Moreover, we identified that WRKY33 functions downstream of CPK5/CPK6 to activate camalexin biosynthetic genes, thereby inducing camalexin biosynthesis. CPK5 and CPK6 interact with WRKY33 and phosphorylate its Thr-229 residue, leading to an increase in the DNA binding ability of WRKY33. By contrast, the MPK3/MPK6-mediated phosphorylation of WRKY33 on its N-terminal Ser residues enhances the transactivation activity of WRKY33. Furthermore, both gain- and loss-of-function genetic analyses demonstrated the cooperative regulation of camalexin biosynthesis by CPK5/CPK6 and MPK3/MPK6. Taken together, these findings indicate that WRKY33 functions as a convergent substrate of CPK5/CPK6 and MPK3/MPK6, which cooperatively regulate camalexin biosynthesis via the differential phospho-regulation of WRKY33 activity.
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影响因子：
11.4
作者：
Eulgem, T;Rushton, PJ;Somssich, IE
通讯作者：
Somssich, IE
影响因子：
20.5
作者：
Boudsocq, Marie;Sheen, Jen
通讯作者：
Sheen, Jen
影响因子：
11.6
作者：
Boettcher, Christoph;Westphal, Lore;Glawischnig, Erich
通讯作者：
Glawischnig, Erich
影响因子：
10.5
作者：
Popescu, Sorina C.;Popescu, George V.;Dinesh-Kumar, Savithramma P.
通讯作者：
Dinesh-Kumar, Savithramma P.
DOI：
10.1073/pnas.0502954102
发表时间：
2005-07-26
影响因子：
11.1
作者：
Ludwig, AA;Saitoh, H;Romeis, T
通讯作者：
Romeis, T