The Nicotiana benthamiana mitogen-activated protein kinase cascade and WRKY transcription factor participate in Nep1(Mo)-triggered plant responses.
The Nicotiana benthamiana mitogen-activated protein kinase cascade and WRKY transcription factor participate in Nep1(Mo)-triggered plant responses.
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DOI：
10.1094/mpmi-11-11-0293
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发表时间：
2012-11
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通讯作者：
Huajian Zhang;Deqing Li;Mei-Mei Wang-Mei;Jiewen Liu;Wenjun Teng;Bao-ling Cheng;Qian Huang;Min Wang;Wenwen Song;S. Dong;Xiaobo Zheng;Zhengguang Zhang
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作者：
Huajian Zhang;Deqing Li;Mei-Mei Wang-Mei;Jiewen Liu;Wenjun Teng;Bao-ling Cheng;Qian Huang;Min Wang;Wenwen Song;S. Dong;Xiaobo Zheng;Zhengguang Zhang
许多细菌、真菌和卵菌物种分泌坏死和乙烯诱导肽1（Nep 1）样蛋白（NLP），其在双子叶植物中触发程序性细胞死亡（PCD）和先天免疫应答。然而，NLP如何诱导这种免疫反应尚不清楚。在这里，我们表明，通过病毒诱导的基因沉默沉默的MAPKKKα-MEK 2-WIPK丝裂原活化蛋白激酶（MAPK）级联的沉默损害过氧化氢的积累和由来自稻瘟病菌的Nep 1（Mo）诱导的PCD。在体外和体内，WIPK与本氏烟草中的转录因子NbWRKY 2相互作用，表明介导Nep 1（Mo）诱导的细胞死亡的效应子途径。出乎意料的是，水杨酸诱导的蛋白激酶（SIPK）和NbWRKY 2沉默的植物表现出受损的Nep 1（Mo）诱导的气孔关闭，减少Nep 1（Mo）促进的保卫细胞中一氧化氮（NO）的产生，并减少Nep 1（Mo）诱导的抗烟草疫霉。实时荧光定量聚合酶链反应表达研究表明，Nep 1（Mo）触发NO积累的MEK 2-WIPK-NbWRKY 2途径可能部分依赖于参与NO合成的硝酸还原酶。总之，这些研究表明，MAPK级联参与Nep 1（Mo）触发的植物反应和MAPK信号与PCD表现出共享和不同的组件与气孔关闭。
Many bacterial, fungal, and oomycete species secrete necrosis and ethylene-inducing peptide 1 (Nep1)-like proteins (NLP) that trigger programmed cell death (PCD) and innate immune responses in dicotyledonous plants. However, how NLP induce such immune responses is not understood. Here, we show that silencing of the MAPKKKα-MEK2-WIPK mitogen-activated protein kinase (MAPK) cascade through virus-induced gene silencing compromises hydrogen peroxide accumulation and PCD induced by Nep1(Mo) from Magnaporthe oryzae. WIPK interacts with NbWRKY2, a transcription factor in Nicotiana benthamiana, in vitro and in vivo, suggesting an effector pathway that mediates Nep1(Mo)-induced cell death. Unexpectedly, salicylic acid-induced protein kinase (SIPK)- and NbWRKY2-silenced plants showed impaired Nep1(Mo)-induced stomatal closure, decreased Nep1(Mo)-promoted nitric oxide (NO) production in guard cells, and a reduction in Nep1(Mo)-induced resistance against Phytophthora nicotianae. Expression studies by real-time polymerase chain reaction suggested that the MEK2-WIPK-NbWRKY2 pathway regulated Nep1(Mo)triggered NO accumulation could be partly dependent on nitrate reductase, which was implicated in NO synthesis. Taken together, these studies demonstrate that the MAPK cascade is involved in Nep1(Mo)-triggered plant responses and MAPK signaling associated with PCD exhibits shared and distinct components with that for stomatal closure.