An effector of a necrotrophic fungal pathogen targets the calcium‐sensing receptor in chloroplasts to inhibit host resistance
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. He...
Saved in:
Published in | Molecular plant pathology Vol. 21; no. 5; pp. 686 - 701 |
---|---|
Main Authors | , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
England
John Wiley & Sons, Inc
01.05.2020
John Wiley and Sons Inc |
Subjects | |
Online Access | Get full text |
ISSN | 1464-6722 1364-3703 |
DOI | 10.1111/mpp.12922 |
Cover
Summary: | 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 Ca2+ 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.
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. |
---|---|
Bibliography: | Funding information This research was supported by the National Nature Science Foundation of China (31571954), the National Key R & D Program of China (2017YFD0200600), Fundamental Research Funds for the Central Universities (2662017PY010), Open Funds of the State Key Laboratory of Agricultural Microbiology (AMLKF201707), and the earmarked fund of China Agriculture Research System (CARS‐13) ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
ISSN: | 1464-6722 1364-3703 |
DOI: | 10.1111/mpp.12922 |