Arabidopsis Clade I TGA Transcription Factors Are Required for Apoplastic Defence Responses

Transcriptional reprogramming during induction of salicylic acid (SA)-mediated defenses is regulated primarily by NPR1 (NON-EXPRESSOR OF PATHOGENESIS RELATED GENES 1), likely through interactions with TGA basic region leucine zipper (bZIP) transcription factors. Using reverse genetics, we have shown that clade I TGA factors (TGA1, TGA4) are required for resistance against virulent, avirulent and nonhost strains of the bacterial pathogen Pseudomonas syringae and act mainly through NPR1-independent pathways. Mutants of clade I TGA factors continue to express near wild-type levels of well-known defence marker genes, such as PR-1, following pathogen challenge but are defective in apoplastic defence responses, including the oxidative burst, callose deposition, and PR-1 protein accumulation. These mutants are more sensitive to the glycosilation inhibitor, tunicamycin, and differentially express genes encoding ER-resident chaperones. Taken together, our data demonstrate that clade I TGA factors contribute to disease resistance against P. syringae through regulating apoplastic defence responses.