An effector of a necrotrophic fungal pathogen targets the calcium‐sensing receptor in chloroplasts to inhibit host resistance. (27th February 2020)

• Record Type: Journal Article
• Authors: Tang, Liguang; Yang, Guogen; Ma, Ming; Liu, Xiaofan; Li, Bo; Xie, Jiatao; Fu, Yanping; Chen, Tao; Yu, Yang; Chen, Weidong; Jiang, Daohong; Cheng, Jiasen
• Is Part Of: Molecular plant pathology. Volume 21:Number 5(2020)
• Page Start: 686
• Page End: 701
• Publication Date: 2020-02-27
• Subjects: calcium‐sensing receptor -- effector -- salicylic acid signalling pathway -- Sclerotinia sclerotiorum -- SsITL; Plant diseases -- Molecular aspects -- Periodicals; Plant-pathogen relationships -- Molecular aspects -- Periodicals; 571.936
• DOI: 10.1111/mpp.12922
• Languages: English
• ISSNs: 1464-6722

Abstract

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 2+ 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 . Abstract : The secretory protein SsITL inhibits salicylic acid accumulation during the early stage of infection by interacting with CAS (calcium‐sensing receptor) and then facilitating S. sclerotiorum infection.