Mode of Action of the Arabidopsis thaliana Phytoalexin Camalexin and Its Role in Arabidopsis-Pathogen Interactions. Elizabeth E. Rogers. Department of Genetics, Harvard Medical School, and Department of Molecular Biology, Massachusetts General Hospital, Boston 02114. Jane Glazebrook, and Frederick M. Ausubel. Department of Genetics, Harvard Medical School, and Department of Molecular Biology, Massachusetts General Hospital, Boston 02114. MPMI 9:748-757. Accepted 30 July 1996. Copyright 1996 The American Phytopathological Society.

The virulent Arabidopsis thaliana pathogen Pseudomonas syringae pv. maculicola strain ES4326 (Psm ES4326) and other gram-negative bacteria are sensitive to camalexin (3-thiazoI-2'-yl-indole), the Arabidopsis phytoalexin. Furthermore, Psm ES4326 is unable to degrade camalexin or to become tolerant to it. Apparently, Psm ES4326 is a successful pathogen even though it elicits synthesis of a host phytoalexin to which it is sensitive. Assays of membrane integrity revealed that, like other phytoalexins, camalexin disrupts bacterial membranes, suggesting that camalexin toxicity is a consequence of membrane disruption. A screen for camalexin-resistant mutants of Psm ES4326 yielded only partially resistant mutants, which displayed partial resistance in both killing and membrane integrity assays. These mutants were also resistant to low concentrations of tetracycline and nalidixic acid, suggesting that they were affected in components of the outer membrane. The mutants were not distinguishable from Psm ES4326 in virulence assays. Camalexin was toxic to Arabidopsis cells growing in tissue culture. However, comparison of the extent of cell death associated with disease symptoms in infected leaves of wild-type Arabidopsis and a camalexin-deficient mutant suggested that camalexin does not contribute significantly to cell death in infected tissue.