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一种真菌效应蛋白通过稳定叶绿体免疫的负调控因子来促进感染。

A fungal effector promotes infection via stabilizing a negative regulatory factor of chloroplast immunity.

作者信息

Xiao Kunqin, Yang Feng, Cui Wenjing, Li Anmo, Rollins Jeffrey A, Guo Jinxin, Sun Xinhua, Wang Fengting, Wang Xiaojie, Xu Xun, Zhang Yanhua, Zhang Xianghui, Liu Jinliang, Pan Hongyu

机构信息

College of Plant Sciences, Jilin University, Changchun, China.

State Key Laboratory of Crop Stress Biology for Arid Areas and College of Plant Protection, Northwest A&F University, Yangling, China.

出版信息

Nat Commun. 2025 Jul 29;16(1):6970. doi: 10.1038/s41467-025-62326-4.

Abstract

Chloroplasts are crucial players in immunity and photosynthesis. However, how chloroplasts arrange the transition between photosynthesis and immunity and how pathogens manipulate this transition remains elusive. Here we report an effector SsCm1 from Sclerotinia sclerotiorum, one of devastating phytopathogenic fungi, inhibits chloroplast immunity and resistance to pathogens, and alleviates photoinhibition in immune state. This is accomplished through stabilizing the conserved chloroplast protein MORF2, which is degraded during immunization and is a suppressor of photoinhibition, cell death, and chloroplast immunity. Overexpression of SsCm1 or MORF2 in plants represses basic immunity and resistance to pathogens, whereas deletion of SsCm1 reduces S. sclerotiorum virulence. Notably, SsCm1 possesses no chorismate mutase activity, which is different from the previously reported Cm effectors. This work reveals a strategy to fine-tune growth-defense balance in chloroplasts by manipulating MORF2, and a pathogenic strategy to subvert the process and promote infection via enzymatically nonfunctional effector stabilizing MORF2.

摘要

叶绿体是免疫和光合作用中的关键参与者。然而,叶绿体如何安排光合作用与免疫之间的转换,以及病原体如何操控这种转换,仍然不清楚。在这里,我们报道了来自核盘菌(一种毁灭性植物病原真菌)的效应蛋白SsCm1,它抑制叶绿体免疫和对病原体的抗性,并减轻免疫状态下的光抑制。这是通过稳定保守的叶绿体蛋白MORF2来实现的,MORF2在免疫过程中会降解,并且是光抑制、细胞死亡和叶绿体免疫的抑制因子。在植物中过表达SsCm1或MORF2会抑制基础免疫和对病原体的抗性,而缺失SsCm1会降低核盘菌的毒力。值得注意的是,SsCm1不具有分支酸变位酶活性,这与先前报道的Cm效应蛋白不同。这项工作揭示了一种通过操控MORF2来微调叶绿体中生长-防御平衡的策略,以及一种通过稳定酶功能缺失的效应蛋白MORF2来颠覆该过程并促进感染的致病策略。

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