Systemic acquired resistance (SAR) is a general defense response in plants that is characterized by the expression of pathogenesis-related (PR) genes. SAR can be induced after a hypersensitive response to an avirulent pathogen or by treatment with either salicylic acid (SA) or 2,6-dichloroisonicotinic acid (INA). To dissect the signal transduction pathway of SAR, we isolated an Arabidopsis mutant that lacks the expression of an SA-, INA-, and pathogen-responsive chimeric reporter gene composed of the 5[prime] untranslated region of an Arabidopsis PR gene, [beta]-1,3-glucanase (BGL2), and the coding region of [beta]-glucuronidase (GUS). This mutant, npr1 (nonexpresser of PR genes), carries a single recessive mutation that abolishes the SAR-responsive expression of other PR genes as well. While SA-, INA-, or avirulent pathogen-induced SAR protects wild-type plants from Pseudomonas syringae infection, the mutant cannot be protected by pretreatment with these inducers. The insensitivity of npr1 to SA, INA, and avirulent pathogens in SAR induction indicates that these inducers share a common signal transduction pathway. Moreover, in npr1, the localized expression of PR genes induced by a virulent Pseudomonas pathogen is disrupted, and the lesion formed is less confined. These results suggest a role for PR genes in preventing the proximal spread of pathogens in addition to their suggested role in SAR.