Heat Shock-Induced Resistance against Pseudomonas syringae pv. Tomato (Okabe) Young et al. Via heat shock transcription factors in tomato

Abstract

We investigated the role of heat shock transcription factors (Hsfs) during induction of defense response by heat-shock treatment (HST) in tomato. Leaf disease symptoms were significantly reduced at 12 and 24 h after HST, consistent with upregulation of pathogenesis-related (PR) genes PR1a2 and PR1b1 peaking at 24 h after treatment. These genes were upregulated at the treatment application site, but not in untreated leaves. In contrast to HST, inoculation of the first leaf induced systemic upregulation of acidic PR genes in uninoculated second leaves. Furthermore, heat shock element motifs were found in upstream regions of PR1a2, PR1b1, Chitinase 3, Chitinase 9, Glucanase A, and Glucanase B genes. Upregulation of HsfA2 and HsfB1 peaked at 6 h after HST, 6 h earlier than salicylic acid accumulation. Foliar spray of heat shock protein 90 (Hsp90) inhibitor geldanamycin (GDA) induced PR gene expression comparable to that after HST. PR gene expression and defense response against Pseudomonas syringae pv. tomato (Pst) decreased when combining HST with Hsfs inhibitor KRIBB11. The Hsfs and PR gene expression induced by heat or GDA, together with the suppression of heat shock-induced resistance (HSIR) against Pst by KRIBB11, suggested a direct contribution of Hsfs to HSIR regulation in tomato.