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Arabidopsis Clade I TGA Transcription Factors Regulate Plant Defenses in an NPR1-Independent Fashion

¹National Research Council Canada, 110 Gymnasium Place, Saskatoon, Saskatchewan, S7N 0W9, Canada; ²Michael Smith Laboratories, University of British Columbia, Vancouver, BC, V6T 1Z4, Canada; ³Department of Biology, University of Saskatchewan, 112 Science Place, Saskatoon, SK, S7N 5E2, Canada; ⁴National Institute of Biological Sciences, Zhongguancun Life Science Park, 7 Science Park Road, Beijing 102206, P.R. China; ⁵Department of Biological Sciences, Brock University, 500 Glenridge Avenue, St. Catharines, ON, L2S 3A1, Canada; ⁶Department of Botany, University of British Columbia, Vancouver, BC, V6T 1Z4, Canada

Transcriptional reprogramming during induction of salicylic acid (SA)-mediated defenses is regulated primarily by NPR1 (NONEXPRESSOR OF PATHOGENESIS-RELATED GENES 1), likely through interactions with TGA bZIP transcription factors. To ascertain the contributions of clade I TGA factors (TGA1 and TGA4) to defense responses, a tga1-1 tga4-1 double mutant was constructed and challenged with Pseudomonas syringae and Hyaloperonospora arabidopsidis. Although the mutant displayed enhanced susceptibility to virulent P. syringae, it was not compromised in systemic acquired resistance against this pathogen or resistance against avirulent H. arabidopsidis. Microarray analysis of nonelicited and SA-treated plants indicated that clade I TGA factors regulate fewer genes than NPR1. Approximately half of TGA-dependent genes were regulated by NPR1 but, in all cases, the direction of change was opposite in the two mutants. In support of the microarray data, the NPR1-independent disease resistance observed in the autoimmune resistance (R) gene mutant snc1 is partly compromised by tga1-1 tga4-1 mutations, and a triple mutant of clade I TGA factors with npr1-1 is more susceptible than either parent. These results suggest that clade I TGA factors are required for resistance against virulent pathogens and avirulent pathogens mediated by at least some R gene specificities, acting substantially through NPR1-independent pathways.