GmMKK4-activated GmMPK6 stimulates GmERF113 to trigger resistance to Phytophthora sojae in soybean
GmMKK4-activated GmMPK6 stimulates GmERF113 to trigger resistance to Phytophthora sojae in soybean
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DOI：
10.1111/tpj.15809
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发表时间：
2022-06-02
期刊：
影响因子：
7.2
通讯作者：
Zhang, Shuzhen
中科院分区：
文献类型：
--
作者：
Gao, Hong;Jiang, Liangyu;Zhang, Shuzhen
大豆疫霉根腐病是由土传病原大豆疫霉引起的世界性大豆病害。大豆疫霉根腐病是大豆生产上的毁灭性病害，因此提高大豆疫霉根腐病的抗性是大豆育种的主要目标。丝裂原活化蛋白激酶（MAPK）级联是将环境刺激转化为细胞反应的重要信号模块。与拟南芥中广泛的研究相比，MAPK级联在大豆抗病性中的分子机制几乎没有阐明。在本研究中，我们发现大豆疫霉菌感染抗病大豆品种‘绥农10’后，有丝分裂原活化蛋白激酶6（GmMPK 6）基因的表达受到强烈的诱导。GmMPK 6基因在大豆中的过表达增强了对大豆疫霉的抗性，而GmMPK 6基因的沉默则导致了相反的表型。在我们试图剖析GmMPK 6在大豆抗疫霉病中的作用时，我们发现MAPK激酶4（GmMKK 4）和ERF转录因子GmERF 113与GmMPK 6物理相互作用，并且我们确定GmMKK 4可以磷酸化并激活GmMPK 6，GmMPK 6随后可以在大豆疫霉感染时磷酸化GmERF 113，表明大豆疫霉可以刺激大豆中的GmMKK 4-GmMPK 6-GmERF 113信号通路。此外，GmMKK 4-GmMPK 6模块对GmERF 113的磷酸化增强了GmERF 113的稳定性、核定位和转录活性，显著增强了防御相关基因GmPR 1和GmPR 10 -1的表达，从而提高了转基因大豆幼苗的抗病性。总之，我们的数据揭示了GmMKK 4-GmMPK 6-GmERF 113级联反应触发大豆对大豆疫霉的抗性，并阐明了MAPK激酶在植物抗病性中的功能。
Phytophthora root and stem rot is a worldwide soybean (Glycine max) disease caused by the soil-borne pathogen Phytophthora sojae. This disease is devastating to soybean production, so improvement of resistance to P. sojae is a major target in soybean breeding. Mitogen-activated protein kinase (MAPK) cascades are important signaling modules that convert environmental stimuli into cellular responses. Compared with extensive studies in Arabidopsis, the molecular mechanism of MAPK cascades in soybean disease resistance is barely elucidated. In this work, we found that the gene expression of mitogen-activated protein kinase 6 (GmMPK6) was potently induced by P. sojae infection in the disease-resistant soybean cultivar 'Suinong 10'. Overexpression of GmMPK6 in soybean resulted in enhanced resistance to P. sojae and silencing of GmMPK6 led to the opposite phenotype. In our attempt to dissect the role of GmMPK6 in soybean resistance to phytophthora disease, we found that MAPK kinase 4 (GmMKK4) and the ERF transcription factor GmERF113 physically interact with GmMPK6, and we determined that GmMKK4 could phosphorylate and activate GmMPK6, which could subsequently phosphorylate GmERF113 upon P. sojae infection, suggesting that P. sojae can stimulate the GmMKK4-GmMPK6-GmERF113 signaling pathway in soybean. Moreover, phosphorylation of GmERF113 by the GmMKK4-GmMPK6 module promoted GmERF113 stability, nuclear localization and transcriptional activity, which significantly enhanced expression of the defense-related genes GmPR1 and GmPR10-1 and hence improved disease resistance of the transgenic soybean seedlings. In all, our data reveal that the GmMKK4-GmMPK6-GmERF113 cascade triggers resistance to P. sojae in soybean and shed light on functions of MAPK kinases in plant disease resistance.