Steven A. Lommel,3
Clifford S. Hogan,2 and
Amy O. Charkowski2
1Department of Biochemistry and Molecular Biology, University of Chicago, 929 E. 57th Street, W225 Chicago, IL 60637, U.S.A.; 2Department of Plant Pathology University of Wisconsin–Madison, 1630 Linden Dr., Madison, WI 53706, U.S.A.; 3Department of Plant Pathology, North Carolina State University, Box 7342, Raleigh, NC 27695-7342, U.S.A.
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Accepted 8 March 2011.
The broad-host-range bacterial soft rot pathogen Pectobacterium carotovorum causes a DspE/F-dependent plant cell death on Nicotiana benthamiana within 24 h postinoculation (hpi) followed by leaf maceration within 48 hpi. P. carotovorum strains with mutations in type III secretion system (T3SS) regulatory and structural genes, including the dspE/F operon, did not cause hypersensitive response (HR)-like cell death and or leaf maceration. A strain with a mutation in the type II secretion system caused HR-like plant cell death but no maceration. P. carotovorum was unable to impede callose deposition in N. benthamiana leaves, suggesting that P. carotovorum does not suppress this basal immunity function. Within 24 hpi, there was callose deposition along leaf veins and examination showed that the pathogen cells were localized along the veins. To further examine HR-like plant cell death induced by P. carotovorum, gene expression profiles in N. benthamiana leaves inoculated with wild-type and mutant P. carotovorum and Pseudomonas syringae strains were compared. The N. benthamiana gene expression profile of leaves infiltrated with Pectobacterium carotovorum was similar to leaves infiltrated with a Pseudomonas syringae T3SS mutant. These data support a model where Pectobacterium carotovorum uses the T3SS to induce plant cell death in order to promote leaf maceration rather than to suppress plant immunity.
© 2011 The American Phytopathological Society