Open AccessdksA Is Required for Intercellular Spread of Shigella flexneri via an RpoS-Independent Mechanism
Author(s) -
Scott A. Mogull,
Laura J. Runyen-Janecky,
Mei Hong,
Shelley M. Payne
Publication year - 2001
Publication title -
infection and immunity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.508
H-Index - 220
eISSN - 1070-6313
pISSN - 0019-9567
DOI - 10.1128/iai.69.9.5742-5751.2001
Subject(s) - rpos , shigella flexneri , biology , mutant , intracellular , cytoplasm , microbiology and biotechnology , virulence , shigella , bacteria , gene , gene expression , salmonella , genetics , escherichia coli , promoter
Pathogenesis of Shigella flexneri is dependent on the ability of the bacterium to invade and spread within epithelial cells. In this study, we identified dksA as a gene necessary for intercellular spread in, but not invasion of, cultured cells. The S. flexneri dksA mutant exhibited sensitivity to acid and oxidative stress, in part due to an effect of DksA on production of RpoS. However, an S. flexneri rpoS mutant formed plaques on tissue culture monolayers, thus excluding DksA regulation of RpoS as the mechanism responsible for the inability of the dksA mutant to spread intercellularly. Intracellular analysis of the dksA mutant indicates that it survived and divided within the Henle cell cytoplasm, but the dksA mutant cells were elongated, and some exhibited filamentation in the intracellular environment. Some of the S. flexneri dksA mutant cells showed aberrant localization of virulence protein IcsA, which may inhibit spread between epithelial cells.