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Actin-related protein MoFim1 modulated the pathogenicity of Magnaporthe oryzae by controlling three MAPK signaling pathways, appressorium formation, and hydrophobicity

文献类型： 外文期刊

作者： Wei, Yun-Yun 1 ; Zhu, Xue-Ming 2 ; Liu, Xiao-Hong 4 ; Lin, Fu-Cheng 2 ; Liang, Shuang 3 ;

作者机构： 1.Zhejiang Shuren Univ, Coll Biol & Environm Engn, Hangzhou 310015, Peoples R China

2.Zhejiang Acad Agr Sci, Inst Plant Protect & Microbiol, Hangzhou 310004, Peoples R China

3.Zhejiang Acad Agr Sci, State Key Lab Managing Biot & Chem Threats Qual &, Hangzhou, Peoples R China

4.Zhejiang Univ, Inst Biotechnol, Lab Rice Biol, Hangzhou 310027, Peoples R China

关键词： Pathogenicity; Autophagy; MAPK signal pathway; Hydrophobicity development; MoFim1

期刊名称：PHYSIOLOGICAL AND MOLECULAR PLANT PATHOLOGY （ 影响因子：2.7； 五年影响因子：2.9 ）

ISSN： 0885-5765

年卷期： 2024 年 132 卷

页码：

收录情况： SCI

摘要： Magnaporthe oryzae seriously threatens rice production and multiple signaling pathways are involved in regulating the pathogenic mechanism of M. oryzae. In M. oryzae, the role of MoFim1 in organizing actin is already identified. The research highlighted its role in other signaling pathways. In this research, MoFIM1 null mutant was produced; resulted in disturbance of three MAPK signaling pathways, hydrophobicity development, and autophagy. The hydrophobicity of mutant Delta Mofim1 was identified to be abnormal by the hydrophobicity testing. Through infection experiments, it was also found that the appressorium-like structure of Delta Mofim1 lost the ability to infect the host cells. Moreover, through the detection of western blot, MoFim1 was involved in three MAPK signaling pathways, and MoFilm1 interacted with MoPmk1. Furthermore, disruption of the gene of MoFIM1 resulted to an influence of autophagy, which certified by fluorescence observation and western blot. Taken together, this research demonstrated that MoFim1 played a crucial role in MAPK signal pathway and autophagy, which laid a more theoretical foundation for improving the pathogenic mechanism of M. oryzae.

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