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一种保守的真菌效应蛋白扰乱钙感知和活性氧稳态以诱导植物细胞死亡。

A conserved fungal effector disturbs Ca sensing and ROS homeostasis to induce plant cell death.

作者信息

Lin Yunlong, Xu Chan, Li Lili, Fan Liqin, Li Rui, He Jiaxin, Li Hongli, Deng Wei, Kang Zhensheng, Li Zhengguo, Cheng Yulin

机构信息

Key Laboratory of Plant Hormones and Molecular Breeding of Chongqing, School of Life Sciences, Chongqing University, Chongqing, China.

Key Laboratory of Plant Genetics and Molecular Breeding, Zhoukou Normal University, Zhoukou, China.

出版信息

Nat Commun. 2025 Apr 14;16(1):3523. doi: 10.1038/s41467-025-58833-z.

DOI:10.1038/s41467-025-58833-z
PMID:40229290
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11997220/
Abstract

Acting as a major Ca sensor, calmodulin (CaM) activates target proteins to regulate a variety of cellular processes. Here, we report that CaM-target binding is disturbed by a fungal virulence effector PdCDIE1 (Penicillium digitatum Cell Death-Inducing Effector 1), which results into reactive oxygen species (ROS)-dependent plant cell death. PdCDIE1 is an evolutionarily conserved fungal effector that exhibits plant cell death-inducing activity and contributes significantly to pathogen virulence. PdCDIE1 interacts with a plant heat shock protein Hsp70 that is antagonistic to ROS-dependent plant cell death. Hsp70 is a bona fide target of CaM and its CaM-binding domain also interacts with N-terminal PdCDIE1. The interaction between CaM and Hsp70 in citrus fruit is disturbed during pathogen infection but recovered during ΔPdCDIE1 mutant infection. Application of a CaM inhibitor and silencing of CaM genes induce plant cell death and high levels of ROS as PdCDIE1 does. These results reveal a molecular framework of effector-triggered susceptibility which integrates Ca sensing and ROS homeostasis to induce plant cell death.

摘要

作为一种主要的钙传感器,钙调蛋白(CaM)激活靶蛋白以调节多种细胞过程。在此,我们报道CaM与靶标的结合受到一种真菌毒力效应蛋白PdCDIE1(指状青霉细胞死亡诱导效应蛋白1)的干扰,这导致活性氧(ROS)依赖性的植物细胞死亡。PdCDIE1是一种进化上保守的真菌效应蛋白,具有诱导植物细胞死亡的活性,并对病原体毒力有显著贡献。PdCDIE1与一种植物热激蛋白Hsp70相互作用,Hsp70对ROS依赖性的植物细胞死亡具有拮抗作用。Hsp70是CaM的一个真正靶标,其CaM结合结构域也与PdCDIE1的N端相互作用。在病原体感染期间,柑橘果实中CaM与Hsp70之间的相互作用受到干扰,但在ΔPdCDIE1突变体感染期间得以恢复。与PdCDIE1一样,应用CaM抑制剂和沉默CaM基因会诱导植物细胞死亡和高水平的ROS。这些结果揭示了一个效应蛋白触发的感病性分子框架,该框架整合了钙感知和ROS稳态以诱导植物细胞死亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39e9/11997220/b66a5a95e74c/41467_2025_58833_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39e9/11997220/9029ef0c3d79/41467_2025_58833_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39e9/11997220/0010563d3c24/41467_2025_58833_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39e9/11997220/b491b9bda8e5/41467_2025_58833_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39e9/11997220/2a9a2564539f/41467_2025_58833_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39e9/11997220/3d441e413921/41467_2025_58833_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39e9/11997220/62129f7b62b3/41467_2025_58833_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39e9/11997220/6c18c2c4c852/41467_2025_58833_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39e9/11997220/b66a5a95e74c/41467_2025_58833_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39e9/11997220/9029ef0c3d79/41467_2025_58833_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39e9/11997220/0010563d3c24/41467_2025_58833_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39e9/11997220/b491b9bda8e5/41467_2025_58833_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39e9/11997220/2a9a2564539f/41467_2025_58833_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39e9/11997220/3d441e413921/41467_2025_58833_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39e9/11997220/62129f7b62b3/41467_2025_58833_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39e9/11997220/6c18c2c4c852/41467_2025_58833_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39e9/11997220/b66a5a95e74c/41467_2025_58833_Fig8_HTML.jpg

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