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稻瘟病菌效应蛋白 MoSPAB1 直接激活水稻 Bsr-d1 表达以促进致病性。

Magnaporthe oryzae effector MoSPAB1 directly activates rice Bsr-d1 expression to facilitate pathogenesis.

机构信息

State Key Laboratory of Crop Gene Exploration and Utilization in Southwest China, Rice Research Institute, Sichuan Agricultural University, Chengdu, Sichuan, 611130, China.

Institute for Advanced Study, Chengdu University, Chengdu, Sichuan, 610106, China.

出版信息

Nat Commun. 2023 Dec 18;14(1):8399. doi: 10.1038/s41467-023-44197-9.

DOI:10.1038/s41467-023-44197-9
PMID:38110425
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10728069/
Abstract

Fungal pathogens typically use secreted effector proteins to suppress host immune activators to facilitate invasion. However, there is rarely evidence supporting the idea that fungal secretory proteins contribute to pathogenesis by transactivating host genes that suppress defense. We previously found that pathogen Magnaporthe oryzae induces rice Bsr-d1 to facilitate infection and hypothesized that a fungal effector mediates this induction. Here, we report that MoSPAB1 secreted by M. oryzae directly binds to the Bsr-d1 promoter to induce its expression, facilitating pathogenesis. Amino acids 103-123 of MoSPAB1 are required for its binding to the Bsr-d1 promoter. Both MoSPAB1 and rice MYBS1 compete for binding to the Bsr-d1 promoter to regulate Bsr-d1 expression. Furthermore, MoSPAB1 homologues are highly conserved among fungi. In particular, Colletotrichum fructicola CfSPAB1 and Colletotrichum sublineola CsSPAB1 activate kiwifruit AcBsr-d1 and sorghum SbBsr-d1 respectively, to facilitate pathogenesis. Taken together, our findings reveal a conserved module that may be widely utilized by fungi to enhance pathogenesis.

摘要

真菌病原体通常利用分泌的效应蛋白来抑制宿主免疫激活物,以促进入侵。然而,很少有证据支持这样一种观点,即真菌分泌蛋白通过反式激活抑制防御的宿主基因来促进发病机制。我们之前发现病原体稻瘟病菌诱导水稻 Bsr-d1 以促进感染,并假设一种真菌效应物介导这种诱导。在这里,我们报告说,稻瘟病菌分泌的 MoSPAB1 直接与 Bsr-d1 启动子结合,诱导其表达,从而促进发病机制。MoSPAB1 氨基酸 103-123 对于其与 Bsr-d1 启动子的结合是必需的。MoSPAB1 和水稻 MYBS1 都竞争与 Bsr-d1 启动子结合,以调节 Bsr-d1 的表达。此外,真菌中的 MoSPAB1 同源物高度保守。特别是,胶孢炭疽菌 CfSPAB1 和细孢炭疽菌 CsSPAB1 分别激活猕猴桃 AcBsr-d1 和高粱 SbBsr-d1,以促进发病机制。总之,我们的研究结果揭示了一个保守的模块,可能被真菌广泛利用来增强致病性。

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