Characterization of an Arabidopsis Mutant That Is Nonresponsive to Inducers of Systemic Acquired Resistance.

TLDR

Systemic acquired resistance (SAR) is a plant defense response marked by induction of pathogenesis‑related genes, which can be triggered by a hypersensitive response, salicylic acid, or 2,6‑dichloroisonicotinic acid. The study aimed to dissect SAR signal transduction by isolating an Arabidopsis mutant lacking expression of an SA‑, INA‑, and pathogen‑responsive chimeric reporter gene. The mutant was identified by screening for loss of a reporter composed of the 5′‑UTR of β‑1,3‑glucanase fused to β‑glucuronidase, revealing a single recessive mutation. The npr1 mutant abolishes SAR‑responsive PR gene expression, fails to gain protection from SA, INA, or avirulent pathogens, shows disrupted localized PR induction and expanded lesions, indicating that PR genes both mediate SAR and limit pathogen spread.

Abstract

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.