Open AccessPectobacterium carotovorum Elicits Plant Cell Death with DspE/F but the P. carotovorum DspE Does Not Suppress Callose or Induce Expression of Plant Genes Early in Plant–Microbe Interactions
Author(s) -
Hyesook Kim,
Phanit Thammarat,
Steven A. Lommel,
Clifford S. Hogan,
Amy O. Charkowski
Publication year - 2011
Publication title -
molecular plant-microbe interactions
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.565
H-Index - 153
eISSN - 1943-7706
pISSN - 0894-0282
DOI - 10.1094/mpmi-06-10-0143
Subject(s) - pectobacterium carotovorum , callose , biology , nicotiana benthamiana , microbiology and biotechnology , type three secretion system , mutant , hypersensitive response , pseudomonas syringae , programmed cell death , pathogen , botany , cell wall , gene , genetics , apoptosis
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.