Abstract
Environmental conditions profoundly affect plant disease development; however, the underlying molecular bases are not well understood. Here we show that elevated temperature significantly increases the susceptibility of Arabidopsis to Pseudomonas syringae pv. tomato (Pst) DC3000 independently of the phyB/PIF thermosensing pathway. Instead, elevated temperature promotes translocation of bacterial effector proteins into plant cells and causes a loss of ICS1-mediated salicylic acid (SA) biosynthesis. Global transcriptome analysis reveals a major temperature-sensitive node of SA signalling, impacting ~60% of benzothiadiazole (BTH)-regulated genes, including ICS1 and the canonical SA marker gene, PR1. Remarkably, BTH can effectively protect Arabidopsis against Pst DC3000 infection at elevated temperature despite the lack of ICS1 and PR1 expression. Our results highlight the broad impact of a major climate condition on the enigmatic molecular interplay between temperature, SA defence and function of a central bacterial virulence system in the context of a widely studied susceptible plant–pathogen interaction.
Highlights
Environmental conditions profoundly affect plant disease development; the underlying molecular bases are not well understood
Temperatures between 27–30 °C are considered ‘moderately elevated’ for Arabidopsis, which is more susceptible to Pst DC3000 infection in this temperature range[18,24,25,26,27]
Periods of elevated temperature vary in nature, to minimize the impact of physiological differences confounding our study, we first assessed the effect of a shorter, 2-day temperature acclimation period on infection of Arabidopsis plants by Pst DC3000
Summary
Environmental conditions profoundly affect plant disease development; the underlying molecular bases are not well understood. Basal defence against Pst DC3000 and induction of SA during effector-triggered immunity have been shown to be compromised at elevated temperature[17,18] It is unclear whether either of these outcomes results from a direct impact of temperature on the SA pathway, as SA-deficient mutants were reported to retain temperature sensitivity during basal defence[18], and loss of effector-triggered immunity-induced SA may be an indirect effect resulting from temperature-mediated loss of upstream resistance (R) protein function. Heat inactivation of phyB results in de-repression of PIF4regulated genes, enabling growth[22] Another recent study suggests that PIF4 mediates defence suppression at elevated temperature; all the pif mutants tested retained temperature-sensitive pathogen growth[24]
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