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脂肪酸延长酶复合物调控细胞膜完整性和稻瘟病菌依赖于隔孢的宿主侵染。

A fatty acid elongase complex regulates cell membrane integrity and septin-dependent host infection by the rice blast fungus.

机构信息

State Key Laboratory of Crop Gene Exploration and Utilization in Southwest China, Rice Research Institute, Sichuan Agricultural University, Chengdu, Sichuan, China.

College of Life Sciences, China West Normal University, Nanchong, Sichuan, China.

出版信息

Mol Plant Pathol. 2024 Jul;25(7):e13494. doi: 10.1111/mpp.13494.

DOI:10.1111/mpp.13494
PMID:39003585
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11246601/
Abstract

Very-long-chain fatty acids (VLCFAs) regulate biophysical properties of cell membranes to determine growth and development of eukaryotes, such as the pathogenesis of the rice blast fungus Magnaporthe oryzae. The fatty acid elongase Elo1 regulates pathogenesis of M. oryzae by modulating VLCFA biosynthesis. However, it remains unknown whether and how Elo1 associates with other factors to regulate VLCFA biosynthesis in fungal pathogens. Here, we identified Ifa38, Phs1 and Tsc13 as interacting proteins of Elo1 by proximity labelling in M. oryzae. Elo1 associated with Ifa38, Phs1 and Tsc13 on the endoplasmic reticulum (ER) membrane to control VLCFA biosynthesis. Targeted gene deletion mutants Δifa38, Δphs1 and Δtsc13 were all similarly impaired as Δelo1 in vegetative growth, conidial morphology, stress responses in ER, cell wall and membrane. These deletion mutants also displayed severe damage in cell membrane integrity and failed to organize the septin ring that is essential for penetration peg formation and pathogenicity. Our study demonstrates that M. oryzae employs a fatty acid elongase complex to regulate VLCFAs for maintaining or remodelling cell membrane structure, which is important for septin-mediated host penetration.

摘要

非常长链脂肪酸 (VLCFAs) 通过调节细胞膜的生物物理特性来决定真核生物的生长和发育,例如稻瘟病菌 Magnaporthe oryzae 的发病机制。脂肪酸延长酶 Elo1 通过调节 VLCFA 生物合成来调节稻瘟病菌的发病机制。然而,Elo1 是否以及如何与其他因素相互作用以调节真菌病原体中的 VLCFA 生物合成仍不清楚。在这里,我们通过 M. oryzae 中的邻近标记鉴定出 Ifa38、Phs1 和 Tsc13 是 Elo1 的相互作用蛋白。Elo1 与内质网 (ER) 膜上的 Ifa38、Phs1 和 Tsc13 结合,以控制 VLCFA 生物合成。靶向基因缺失突变体 Δifa38、Δphs1 和 Δtsc13 在营养生长、分生孢子形态、ER、细胞壁和膜中的应激反应方面与 Δelo1 相似受损。这些缺失突变体在细胞膜完整性方面也受到严重损害,无法组织用于穿透钉形成和致病性所必需的隔膜环。我们的研究表明,稻瘟病菌使用脂肪酸延长酶复合物来调节 VLCFAs 以维持或重塑细胞膜结构,这对于隔膜介导的宿主穿透很重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c554/11246601/0ec601d66d53/MPP-25-e13494-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c554/11246601/dd509c47f820/MPP-25-e13494-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c554/11246601/ff6ad9f1494f/MPP-25-e13494-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c554/11246601/dcb8a0d89908/MPP-25-e13494-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c554/11246601/0ec601d66d53/MPP-25-e13494-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c554/11246601/dd509c47f820/MPP-25-e13494-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c554/11246601/ff6ad9f1494f/MPP-25-e13494-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c554/11246601/dcb8a0d89908/MPP-25-e13494-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c554/11246601/0ec601d66d53/MPP-25-e13494-g001.jpg

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