title: Suppression and Restoration of Lesion Formation in Arabidopsis lsd Mutants.
abstract: Systemic acquired resistance (SAR) is a broad-spectrum, systemic defense response that is activated in many plant species after pathogen infection. We have previously described Arabidopsis mutants that constitutively express SAR and concomitantly develop lesions simulating disease (lsd). Here, we describe two new mutants, lsd6 and lsd7, that develop spontaneous necrotic lesions and possess elevated levels of salicylic acid (SA) as well as heightened disease resistance, similar to the previously characterized lsd and accelerated cell death (acd2) mutants. Genetic analysis of lsd6 and lsd7 showed that the mutant phenotypes segregated as simple dominant traits. When crossed with transgenic Arabidopsis 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, suggesting 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 signal transduction pathway leading to SAR and disease resistance are potentiated by later events, suggesting feedback control of lesion formation.
authors.affiliation: Agricultural Biotechnology Research Unit, Ciba Geigy Corporation, P.O. Box 12257, Research Triangle Park, North Carolina 27709-2257.
authors.forename: K.
authors.initials: K
authors.lastname: Weymann
authors.forename: M.
authors.initials: M
authors.lastname: Hunt
authors.forename: S.
authors.initials: S
authors.lastname: Uknes
authors.forename: U.
authors.initials: U
authors.lastname: Neuenschwander
authors.forename: K.
authors.initials: K
authors.lastname: Lawton
authors.forename: H. Y.
authors.initials: HY
authors.lastname: Steiner
authors.forename: J.
authors.initials: J
authors.lastname: Ryals