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Infection and Immunity, September 2001, p. 5742-5751, Vol. 69, No. 9
Section of Molecular Genetics and
Microbiology and Institute for Cellular and Molecular Biology, The
University of Texas at Austin, Austin, Texas 78712-1095
Received 1 February 2001/Returned for modification 13 April
2001/Accepted 31 May 2001
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.
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.69.9.5742-5751.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
dksA Is Required for Intercellular
Spread of Shigella flexneri via an
RpoS-Independent Mechanism
and
*
Corresponding author. Mailing address: Section of
Molecular Genetics and Microbiology, The University of Texas, Austin,
TX 78712-1095. Phone: (512) 471-9258. Fax: (512) 471-7088. E-mail: payne{at}mail.utexas.edu.
Present address: DoubleTwist Inc., Oakland, CA 94612.
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