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Activation-Dependent Destruction of a Co-receptor by a Pseudomonas syringae Effector Dampens Plant Immunity
Lei Li, Panya Kim, Liping Yu, Gaihong Cai, She Chen, James R. Alfano, Jian-Min Zhou
Cell Host Microbe
Abstract
The Arabidopsis immune receptor FLS2 and co-receptor BAK1 perceive the bacterial flagellin epitope flg22 to activate plant immunity. To prevent this response, phytopathogenic bacteria deploy a repertoire of effector proteins to perturb immune signaling. However, the effector-induced perturbation is often sensed by the host, triggering another layer of immunity. We report that the Pseudomonas syringae effector HopB1 acts as a protease to cleave immune-activated BAK1. Prior to activation, HopB1 constitutively interacts with FLS2. Upon activation by flg22, BAK1 is recruited to the FLS2-HopB1 complex and is phosphorylated at Thr455. HopB1 then specifically cleaves BAK1 between Arg297 and Gly298 to inhibit FLS2 signaling. Although perturbation of BAK1 is known to trigger increased immune responses in plants, the HopB1-mediated cleavage of BAK1 leads to enhanced virulence, but not disease resistance. This study thus reveals a virulence strategy by which a pathogen effector attacks the plant immune system with minimal host perturbation.
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论文编号: |
DOI:10.1016/j.chom.2016.09.007 |
论文题目: |
Activation-Dependent Destruction of a Co-receptor by a Pseudomonas syringae Effector Dampens Plant Immunity |
英文论文题目: |
Activation-Dependent Destruction of a Co-receptor by a Pseudomonas syringae Effector Dampens Plant Immunity |
第一作者: |
Lei Li, Panya Kim, Liping Yu, Gaihong Cai, She Chen, James R. Alfano, Jian-Min Zhou |
英文第一作者: |
Lei Li, Panya Kim, Liping Yu, Gaihong Cai, She Chen, James R. Alfano, Jian-Min Zhou |
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2016-10-14 |
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摘要: |
The Arabidopsis immune receptor FLS2 and co-receptor BAK1 perceive the bacterial flagellin epitope flg22 to activate plant immunity. To prevent this response, phytopathogenic bacteria deploy a repertoire of effector proteins to perturb immune signaling. However, the effector-induced perturbation is often sensed by the host, triggering another layer of immunity. We report that the Pseudomonas syringae effector HopB1 acts as a protease to cleave immune-activated BAK1. Prior to activation, HopB1 constitutively interacts with FLS2. Upon activation by flg22, BAK1 is recruited to the FLS2-HopB1 complex and is phosphorylated at Thr455. HopB1 then specifically cleaves BAK1 between Arg297 and Gly298 to inhibit FLS2 signaling. Although perturbation of BAK1 is known to trigger increased immune responses in plants, the HopB1-mediated cleavage of BAK1 leads to enhanced virulence, but not disease resistance. This study thus reveals a virulence strategy by which a pathogen effector attacks the plant immune system with minimal host perturbation. |
英文摘要: |
The Arabidopsis immune receptor FLS2 and co-receptor BAK1 perceive the bacterial flagellin epitope flg22 to activate plant immunity. To prevent this response, phytopathogenic bacteria deploy a repertoire of effector proteins to perturb immune signaling. However, the effector-induced perturbation is often sensed by the host, triggering another layer of immunity. We report that the Pseudomonas syringae effector HopB1 acts as a protease to cleave immune-activated BAK1. Prior to activation, HopB1 constitutively interacts with FLS2. Upon activation by flg22, BAK1 is recruited to the FLS2-HopB1 complex and is phosphorylated at Thr455. HopB1 then specifically cleaves BAK1 between Arg297 and Gly298 to inhibit FLS2 signaling. Although perturbation of BAK1 is known to trigger increased immune responses in plants, the HopB1-mediated cleavage of BAK1 leads to enhanced virulence, but not disease resistance. This study thus reveals a virulence strategy by which a pathogen effector attacks the plant immune system with minimal host perturbation. |
刊物名称: |
Cell Host Microbe |
英文刊物名称: |
Cell Host Microbe |
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Lei Li, Panya Kim, Liping Yu, Gaihong Cai, She Chen, James R. Alfano, Jian-Min Zhou. Activation-Dependent Destruction of a Co-receptor by a Pseudomonas syringae Effector Dampens Plant Immunity. Cell Host Microbe. DOI:10.1016/j.chom.2016.09.007 |
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