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The exodomain of the impaired oomycete susceptibility 1 receptor mediates both endoplasmic reticulum stress responses and abscisic acid signalling during downy mildew infection of Arabidopsis

The phytohormone abscisic acid (ABA) regulates cell growth and plant development, and contributes to defence responses to pathogens. We previously showed that the Arabidopsis malectin‐like domain leucine‐rich repeat receptor‐like kinase (MLD‐LRR‐RLK) impaired oomycete susceptibility 1 (IOS1) attenua...

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Detalles Bibliográficos
Autores principales: Giordano, Laïla, Schimmerling, Marion, Panabières, Franck, Allasia, Valérie, Keller, Harald
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9644275/
https://www.ncbi.nlm.nih.gov/pubmed/36103373
http://dx.doi.org/10.1111/mpp.13265
Descripción
Sumario:The phytohormone abscisic acid (ABA) regulates cell growth and plant development, and contributes to defence responses to pathogens. We previously showed that the Arabidopsis malectin‐like domain leucine‐rich repeat receptor‐like kinase (MLD‐LRR‐RLK) impaired oomycete susceptibility 1 (IOS1) attenuates ABA signalling during infection with the oomycete downy mildew pathogen Hyaloperonospora arabidopsidis. The exodomain of IOS1 with its MLD retains the receptor in the endoplasmic reticulum (ER), where it interacts with the ribophorin HAP6 to dampen a pathogen‐induced ER stress response called the unfolded protein response (UPR). The down‐regulation of both ABA and UPR signalling probably provides the pathogen with an advantage for infection. Here, we show that ABA‐related phenotypes of the ios1‐1 mutant, such as up‐regulated expression of ABA‐responsive genes and hypersensitivity to exogenous ABA application, were reverted by expression of the IOS1 exodomain in the mutant background. Furthermore, knockdown mutants for ER‐resident HAP6 showed similarly reduced UPR and ABA signalling, indicating that HAP6 positively regulates both pathways. Our data suggest that the IOS1 exodomain and HAP6 contribute in the ER to the IOS1‐mediated interference with ABA and UPR signalling.