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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.

Dual impact of elevated temperature on plant defence and bacterial virulence in Arabidopsis