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The Arabidopsis thaliana LysM‐containing Receptor‐Like Kinase 2 is required for elicitor‐induced resistance to pathogens

In Arabidopsis thaliana, perception of chitin from fungal cell walls is mediated by three LysM‐containing Receptor‐Like Kinases (LYKs): CERK1, which is absolutely required for chitin perception, and LYK4 and LYK5, which act redundantly. The role in plant innate immunity of a fourth LYK protein, LYK2...

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Detalles Bibliográficos
Autores principales: Giovannoni, Moira, Lironi, Damiano, Marti, Lucia, Paparella, Chiara, Vecchi, Valeria, Gust, Andrea A., De Lorenzo, Giulia, Nürnberger, Thorsten, Ferrari, Simone
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley & Sons, Ltd. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9293440/
https://www.ncbi.nlm.nih.gov/pubmed/34558681
http://dx.doi.org/10.1111/pce.14192
Descripción
Sumario:In Arabidopsis thaliana, perception of chitin from fungal cell walls is mediated by three LysM‐containing Receptor‐Like Kinases (LYKs): CERK1, which is absolutely required for chitin perception, and LYK4 and LYK5, which act redundantly. The role in plant innate immunity of a fourth LYK protein, LYK2, is currently not known. Here we show that CERK1, LYK2 and LYK5 are dispensable for basal susceptibility to B. cinerea but are necessary for chitin‐induced resistance to this pathogen. LYK2 is dispensable for chitin perception and early signalling events, though it contributes to callose deposition induced by this elicitor. Notably, LYK2 is also necessary for enhanced resistance to B. cinerea and Pseudomonas syringae induced by flagellin and for elicitor‐induced priming of defence gene expression during fungal infection. Consistently, overexpression of LYK2 enhances resistance to B. cinerea and P. syringae and results in increased expression of defence‐related genes during fungal infection. LYK2 appears to be required to establish a primed state in plants exposed to biotic elicitors, ensuring a robust resistance to subsequent pathogen infections.