Poster: Plant Pathogen/Symbiont Interactions

Abs # 751: NPR2: A Novel Arabidopsis Defense Response Gene

Presenter:	Racki, Lisa R, racki@fas.harvard.edu
Authors	Racki, Lisa R (A)   Yorgey, Pete  (B)   Dewdney, Julia  (C) (D)  Ausubel, Frederick M (C) (D)
Affiliations:	(A): Harvard College (B): Microbia Inc. (C): Department of Genetics, Harvard Medical School (D): Department of Molecular Biology, Massachusetts General Hospital

The induction of known pathogen-related genes in plants by salicylic acid (SA), a known inducer of immune response genes PR-1, BGL2, and PR-5, is blocked in npr1 mutants. The PR-1, BGL2, and PR-5 genes are used as markers for Systemic Acquired Resistance (SAR) because they are induced systemically in response to a range of necrotizing pathogens. One interesting but unexplained finding was that while local defense gene induction by salicylic acid (SA) was blocked in npr1 mutants, inoculation of npr1 mutants with Pseudomonas syringae or Erysiphe orontii still resulted in local defense gene induction, especially BGL2 induction. This finding suggested the existence of an NPR1-independent pathway to Local Acquired Resistance (LAR). To identify components of this putative pathway, Arabidopsis thaliana mutants were identified that failed to activate a BGL2-GUS reporter construct in response to P. syringae infection in an npr1 mutant background. One gene identified in this screen, NPR2, appears to be involved in NPR1-independent expression of BGL2. In the recessive npr2 mutant, neither pathogens nor SA induce BGL2 expression, suggesting that the NPR2 gene is required for both SA-dependent and pathogen-dependent BGL2 expression. The npr2 mutant exhibits altered expression of other PR-genes including constitutive PR1 expression which is blocked in the npr1 npr2 double mutant, as well as an unusual expression pattern of the JA/ET pathway response element PDF1.2. The npr2 mutant is non-responsive to JA in inducing PDF1.2, but the npr1 npr2 double mutant demonstrates increased induction of PDF1.2 with JA. Thus, NPR2 appears to provide a link between the JA/ET pathway and NPR1-dependent and independent PR-gene expression.