A key sphingolipid pathway gene, MoDES1, regulates conidiation, virulence and plasma membrane tension in Magnaporthe oryzae
文献类型: 外文期刊
第一作者: Wang, Lei
作者: Wang, Lei;Zhang, Xiaozhi;Lin, Fucheng;Zhu, Xueming;Li, Lin;Bao, Jiandong;Lin, Fucheng;Zhu, Xueming;Lin, Fucheng
作者机构:
关键词: Magnaporthe oryzae; MoDES1; Sphingolipid; Pathogenic fungi; Lipid homeostasis; PM tension
期刊名称:MICROBIOLOGICAL RESEARCH ( 影响因子:6.1; 五年影响因子:6.5 )
ISSN: 0944-5013
年卷期: 2024 年 279 卷
页码:
收录情况: SCI
摘要: Rice blast, caused by the plant pathogenic fungus Magnaporthe oryzae, is a destructive disaster all over the earth that causes enormous losses in crop production. Sphingolipid, an important biological cell membrane lipid, is an essential structural component in the plasma membrane (PM) and has several biological functions, including cell mitosis, apoptosis, stress resistance, and signal transduction. Previous studies have suggested that sphingolipid and its derivatives play essential roles in the virulence of plant pathogenic fungi. However, the functions of sphingolipid biosynthesis-related proteins are not fully understood. In this article, we identified a key sphingolipid synthesis enzyme, MoDes1, and found that it is engaged in cell development and pathogenicity in M. oryzae. Deletion of MoDES1 gave rise to pleiotropic defects in vegetative growth, conidiation, plant penetration, and pathogenicity. MoDes1 is also required for lipid homeostasis and participates in the cell wall integrity (CWI) and Osm1-MAPK pathways. Notably, our results showed that there is negative feedback in the TORC2 signaling pathway to compensate for the decreased sphingolipid level due to the knockout of MoDES1 by regulating the phosphorylated Ypk1 level and PM tension. Furthermore, protein structure building has shown that MoDes1 is a potential drug target. These findings further refine the function of Des1 and deepen our understanding of the sphingolipid biosynthesis pathway in M. oryzae, laying a foundation for developing novel and specific drugs for rice blast control.
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