The Arabidopsis ssi1 mutation restores pathogenesis-related gene expression in npr1 plants and renders defensin gene expression salicylic acid dependent

The Arabidopsis NPR1 gene was previously shown to be required for the salic ylic acid (SA)- and benzothiadiazole (BTH)-induced expression of pathogenes is-related (PR) genes and systemic acquired resistance. The dominant ssi1 ( for suppressor of SA insensitivity) mutation characterized in this study de fines a new component of the sA signal transduction pathway that bypasses t he requirement of NPR1 for expression of the PR genes and disease resistanc e. The ssi1 mutation caused PR (PR-1, BGL2 [PR-2], and PR-5) genes to be co nstitutively expressed and restored resistance to an avirulent strain of Ps eudomonas syringae pv tomato in npr1-6 (previously called sail) mutant plan ts. In addition, ssi1 plants were small, spontaneously developed hypersensi tive response-like lesions, accumulated elevated levels of SA, and constitu tively expressed the antimicrobial defensin gene PDF1.2. The phenotypes of the ssi1 mutant are SA dependent. When SA accumulation was prevented in ssi 1 npr1-5 plants by expressing the SA-degrading salicylate hydroxylase (nahG ) gene, all of the phenotypes associated with the ssi1 mutation were suppre ssed. However, lesion formation and expression of the PR genes were restore d in these plants by the application of BTH. Interestingly, expression of P DF1.2, which previously has been shown to be SA independent but jasmonic ac id and ethylene dependent, was also suppressed in ssi1 npr1-5 plants by the nahG gene. Furthermore, exogenous application of BTH restored PDF1.2 expre ssion in these plants. Our results suggest that SSI1 may function as a swit ch modulating cross-talk between the SA- and jasmonic acid/ethylene-mediate d defense signal transduction pathways.