Suppression and Restoration of Lesion Formation in

Systemic acquired resistance (SAR) is a broad-spectrum, systemic defense response that is activated in many plant spe-cies after pathogen infection. We have previously described Arabidopsis mutants that constitutively express SAR and concomitantly develop Lesions amulating gsease (Isd). Here, we describe two new mutants, lsd6 and lsd7, that de-velop spontaneous necrotic lesions and possess elevated levels of salicylic acid (SA) as'well as heightened disease resis-tance, similar to the previously characterized lsd and gccelerated cell death (acd2) mutants. Genetic analysis of lsd6 and lsd7 showed that the mutant phenotypes segregated as simple dominant traits. When crossed with transgenic Arabidop sis plants containing the SA-degrading enzyme salicylate hydroxylase, the F1 progeny showed suppression of both SAR gene expression and resistance. In addition, salicylate hydroxylase suppressed lesion formation in the F1 progeny, sug-gesting that SA or some SA-dependent process may have a role in pathogen-associated cell death. Surprisingly, lesions were restored in the lsd6 F1 progeny after the application of either 2,6-dichloroisonicotinic acid or SA. Lesions were not restored by treatment with either compound in the lsd7 F1 plants. Our findings demonstrate that steps early in the sig-na1 transduction pathway leading to SAR and disease resistance are potentiated by later events, suggesting feedback control of lesion formation.