A NOVEL SIGNALING PATHWAY CONTROLLING INDUCED SYSTEMIC RESISTANCE IN ARABIDOPSIS

Plants have the ability to acquire an enhanced level of resistance to pathogen attack after being exposed to specific biotic stimuli. In Ara bidopsis, nonpathogenic, root-colonizing Pseudomonas fluorescens bacte ria trigger an induced systemic resistance (ISR) response against infe ction by the bacterial leaf pathogen P. syringae pv tomato. In contras t to classic, pathogen-induced systemic acquired resistance (SAR), thi s rhizobacteria-mediated ISR response is independent of salicylic acid accumulation and pathogenesis-related gene activation. Using the jasm onate response mutantjar1, the ethylene response mutant etr1, and the SAR regulatory mutant npr1, we demonstrate that signal transduction le ading to P. fluorescens WCS417r-mediated ISR requires responsiveness t o jasmonate and ethylene and is dependent on NPR1. Similar to P. fluor escens WCS417r, methyl jasmonate and the ethylene precursor 1-aminocyc lopropane-1-carboxylate were effective in inducing resistance against P.s. tomato in salicylic acid-nonaccumulating NahG plants. Moreover, m ethyl jasmonate-induced protection was blocked in jar1, efr1, and npr1 plants, whereas 1-aminocyclopropane-1-carboxylate-induced protection was affected in etr1 and npr1 plants but not in jar1 plants. Hence, we postulate that rhizobacteria-mediated ISR follows a novel signaling p athway in which components from the jasmonate and ethylene response ar e engaged successively to trigger a defense reaction that, like SAR, i s regulated by NPR1. We provide evidence that the processes downstream of NPR1 in the ISR pathway are divergent from those in the SAR pathwa y, indicating that NPR1 differentially regulates defense responses, de pending on the signals that are elicited during induction of resistanc e.