MoPpe1 partners with MoSap1 to mediate TOR and cell wall integrity signalling in growth and pathogenicity of the rice blast fungus Magnaporthe oryzae.

MoPpe1 partners with MoSap1 to mediate TOR and cell wall integrity signalling in growth and pathogenicity of the rice blast fungus Magnaporthe oryzae.
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MoPpe1 与 MoSap1 合作,介导稻瘟病菌 Magnaporthe oryzae 生长和致病性中的 TOR 和细胞壁完整性信号传导

DOI:
10.1111/1462-2920.14421
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发表时间:
2018-11
影响因子:
5.1
通讯作者:
Zhang Z
Zhang Z
中科院分区:
生物学2区
文献类型:
--
作者:
Qian B;Liu X;Jia J;Cai Y;Chen C;Zhang H;Zheng X;Wang P;Zhang Z

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在稻瘟病菌中,细胞壁完整性(CWI)信号传导途径控制细胞壁响应于外部线索的变化,并且正常的CWI信号传导对于附着胞功能和致病性至关重要。我们以前的特点是丝裂原活化蛋白激酶(MAPK)激酶MoMkk 1作为一个不可分割的组成部分的CWI途径。使用亲和纯化的方法,我们已经确定MoMkk 1相互作用MoPpe 1作为酿酒酵母丝氨酸/苏氨酸蛋白磷酸酶Sit 4/Ppe 1的同源物。我们发现MoPpe 1是营养生长、分生孢子形成和完全毒力所必需的。此外,我们发现MoPpe 1与MoSap 1相互作用,MoSap 1是一种功能与MoPpe 1相似的蛋白质。有趣的是,我们发现MoPpe 1-MoSap 1相互作用与CWI和雷帕霉素靶点(TOR)通路有关。我们提出的证据表明,MoPpe 1和MoSap 1的功能作为一个接头复合物连接CWI和TOR信号转导和TOR途径的激活导致抑制CWI信号转导,导致附着胞功能和致病性的缺陷。综上所述,我们的研究不仅揭示了MoMkk 1-MoPpe 1-MoSap 1相互作用在稻瘟病菌生长和致病性中的重要功能,而且还突出了涉及保守但新颖的CWI和TOR信号转导调控机制的调控网络的复杂性。
In the rice blast fungus Magnaporthe oryzae, the cell wall integrity (CWI) signalling pathway governs cell wall changes in response to external cues and normal CWI signalling is critical for appressorium function and pathogenicity. We previously characterized the mitogen-activated protein kinase (MAPK) kinase MoMkk1 as an integral component of the CWI pathway. Using the affinity purification approach, we have identified MoMkk1-interacting MoPpe1 as a homologue of Saccharomyces cerevisiae serine/threonine protein phosphatase Sit4/Ppe1. We found that MoPpe1 is required for vegetative growth, conidiation and full virulence. In addition, we found that MoPpe1 interacts with MoSap1, a protein with functions similar to MoPpe1. Intriguingly, we found that MoPpe1-MoSap1 interaction is related to CWI and target of rapamycin (TOR) pathways. We presented evidence suggesting that MoPpe1 and MoSap1 function as an adaptor complex linking CWI and TOR signalling and that the activation of the TOR pathway leads to suppression of CWI signalling, resulting in defects in appressorium function and pathogenicity. Taken together, our studies not only reveal important functions of MoMkk1-MoPpe1-MoSap1 interactions in growth and pathogenicity of the blast fungus, but also highlight the complexity of regulatory networks involving conserved yet novel regulatory mechanisms of CWI and TOR signalling.
DOI: 10.1105/tpc.110.075937
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