Temperature regulation of salicylic acid-mediated defense in Arabidopsis thaliana
B. HUOT (1), A. Velásquez (2), E. Hubbard (2), J. Pulman (3), J. Yao (4), K. Childs (3), K. Tsuda (6), B. Montgomery (7), S. He (8) (1) DOE-Plant Research Laboratory, Cell and Molecular Biology Program, Michigan State University, U.S.A.; (2) DOE-Plant Research Laboratory, Michigan State University, U.S.A.; (3) Plant Biology Department, Center for Genomics Enabled Plant Science, Michigan State University, U.S.A.; (4) Department of Biological Sciences, Western Michigan University, U.S.A.; (5) Plant Biology Department, Center for Genomics Enabled Plant Science, Michigan State University, U.S.A.; (6) Department of Plant-Microbe Interactions, Max Planck Institute for Plant Breeding Research, Germany; (7) DOE-Plant Research Laboratory, Department of Biochemistry and Molecular Biology, Michigan State University, U.S.A.; (8) DOE-Plant Research Laboratory, Howard Hughes Medical Institute-Gordon and Betty Moore Foundation, Michigan State University, U.S.A.

Environmental conditions greatly effect plant disease progression; however, the mechanisms regulating plant responses to combined abiotic and biotic stresses are largely unknown. We initiated a study to identify the molecular mechanism(s) underlying the effect of moderately elevated temperature (ET; 30?C) on salicylic acid (SA)-mediated defense in Arabidopsis thaliana and to determine how such modulation affects Pseudomonas syringae pv. tomato DC3000 (DC3000) infection. We found that enhanced susceptibility of Arabidopsis to DC3000 at ET is correlated with loss of SA production and PATHOGENESIS RELATED1 (PR1) gene expression. Surprisingly, protection by the SA analog, benzothiadiazole (BTH), persisted at ET in the absence of SA and PR1. Global transcriptional analysis confirmed an overall negative impact of ET on BTH-regulated genes, but also revealed a subset of genes uniquely induced by BTH at ET. Hormone crosstalk is implicated in regulation of these temperature-dependent, BTH-induced genes. Investigation into the mechanism of BTH-mediated protection at ET revealed a novel role of BTH in reducing type III effector translocation. The master regulator of SA signaling, NONEXPRESSOR OF PR GENES1 (NPR1), was found to be required for protection against bacterial multiplication and reduction of type III effector translocation at ET. Our results shed light on the enigmatic molecular interplay between temperature, SA signaling and function of a central bacterial virulence system.

Abstract Number: P16-453
Session Type: Poster