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Light prevents pathogen-induced aqueous microenvironments via potentiation of salicylic acid signaling

Many plant pathogens induce water-soaked lesions in infected tissues. In the case of Pseudomonas syringae (Pst), water-soaking effectors stimulate abscisic acid (ABA) production and signaling, resulting in stomatal closure. This reduces transpiration, increases water accumulation, and induces an apo...

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Detalles Bibliográficos
Autores principales: Lajeunesse, Gaële, Roussin-Léveillée, Charles, Boutin, Sophie, Fortin, Élodie, Laforest-Lapointe, Isabelle, Moffett, Peter
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9911384/
https://www.ncbi.nlm.nih.gov/pubmed/36759607
http://dx.doi.org/10.1038/s41467-023-36382-7
Descripción
Sumario:Many plant pathogens induce water-soaked lesions in infected tissues. In the case of Pseudomonas syringae (Pst), water-soaking effectors stimulate abscisic acid (ABA) production and signaling, resulting in stomatal closure. This reduces transpiration, increases water accumulation, and induces an apoplastic microenvironment favorable for bacterial growth. Stomata are sensitive to environmental conditions, including light. Here, we show that a period of darkness is required for water-soaking, and that a constant light regime abrogates stomatal closure by Pst. We find that constant light induces resistance to Pst, and that this effect requires salicylic acid (SA). Constant light did not alter effector-induced accumulation of ABA, but induced greater SA production, promoting stomatal opening despite the presence of ABA. Furthermore, application of a SA analog was sufficient to prevent pathogen-induced stomatal closure and water-soaking. Our results suggest potential approaches for interfering with a common virulence strategy, as well as providing a physiological mechanism by which SA functions in defense against pathogens.