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一种坏死型真菌病原体的效应子靶向质体中的钙敏感受体,以抑制宿主抗性。

An effector of a necrotrophic fungal pathogen targets the calcium-sensing receptor in chloroplasts to inhibit host resistance.

机构信息

State Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, Hubei Province, China.

The Provincial Key Lab of Plant Pathology of Hubei Province, College of Plant Science and Technology, Huazhong Agricultural University, Wuhan, Hubei Province, China.

出版信息

Mol Plant Pathol. 2020 May;21(5):686-701. doi: 10.1111/mpp.12922. Epub 2020 Feb 27.

DOI:10.1111/mpp.12922
PMID:32105402
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7170781/
Abstract

SsITL, a secretory protein of the necrotrophic phytopathogen Sclerotinia sclerotiorum, was previously reported to suppress host immunity at the early stages of infection. However, the molecular mechanism that SsITL uses to inhibit plant defence against S. sclerotiorum has not yet been elucidated. Here, we report that SsITL interacted with a chloroplast-localized calcium-sensing receptor, CAS, in chloroplasts. We found that CAS is a positive regulator of the salicylic acid signalling pathway in plant immunity to S. sclerotiorum and CAS-mediated resistance against S. sclerotiorum depends on Ca signalling. Furthermore, we showed that SsITL could interfere with the plant salicylic acid (SA) signalling pathway and SsITL-expressing transgenic plants were more susceptible to S. sclerotiorum. However, truncated SsITLs (SsITL-NT1 or SsITL-CT1) that lost the ability to interact with CAS do not affect plant resistance to S. sclerotiorum. Taken together, our findings reveal that SsITL inhibits SA accumulation during the early stage of infection by interacting with CAS and then facilitating the infection by S. sclerotiorum.

摘要

SsITL 是一种坏死型植物病原菌核盘菌的分泌蛋白,先前的研究表明其在感染早期抑制宿主免疫。然而,SsITL 抑制植物防御核盘菌的分子机制尚不清楚。本研究报告 SsITL 与定位于叶绿体的钙敏感受体 CAS 在叶绿体中相互作用。我们发现 CAS 是植物对核盘菌免疫中水杨酸信号通路的正调控因子,CAS 介导的核盘菌抗性依赖于钙信号。此外,我们表明 SsITL 可以干扰植物水杨酸(SA)信号通路,SsITL 表达的转基因植物对核盘菌更敏感。然而,失去与 CAS 相互作用能力的截短 SsITLs(SsITL-NT1 或 SsITL-CT1)并不影响植物对核盘菌的抗性。综上所述,本研究结果揭示了 SsITL 通过与 CAS 相互作用抑制感染早期的 SA 积累,从而促进核盘菌的侵染。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da7b/7170781/561d1ccb7829/MPP-21-686-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da7b/7170781/11c56354dd1b/MPP-21-686-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da7b/7170781/a152bfd42729/MPP-21-686-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da7b/7170781/3ac4d66e6776/MPP-21-686-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da7b/7170781/561d1ccb7829/MPP-21-686-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da7b/7170781/11c56354dd1b/MPP-21-686-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da7b/7170781/a152bfd42729/MPP-21-686-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da7b/7170781/3ac4d66e6776/MPP-21-686-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da7b/7170781/561d1ccb7829/MPP-21-686-g005.jpg

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