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Infection and Immunity, March 2008, p. 1083-1092, Vol. 76, No. 3
0019-9567/08/$08.00+0     doi:10.1128/IAI.01211-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Role and Regulation of Iron-Sulfur Cluster Biosynthesis Genes in Shigella flexneri Virulence{triangledown}

Laura Runyen-Janecky,* Aaron Daugherty, Benjamin Lloyd, Christopher Wellington, Haig Eskandarian, and Matthew Sagransky

Department of Biology, University of Richmond, Richmond, Virginia 23173

Received 4 September 2007/ Returned for modification 10 October 2007/ Accepted 2 January 2008

Shigella flexneri, a causative agent of bacterial dysentery, possesses two predicted iron-sulfur cluster biosynthesis systems called Suf and Isc. S. flexneri strains containing deletion mutations in the entire suf operon (UR011) or the iscSUA genes (UR022) were constructed. Both mutants were defective in surviving exposure to oxidative stress. The suf mutant showed growth that was comparable to that of the parental strain in both iron-replete and iron-limiting media; however, the isc mutant showed reduced growth, relative to the parental strain, in both media. Although the suf mutant formed wild-type plaques on Henle cell monolayers, the isc mutant was unable to form plaques on Henle cell monolayers because the strain was noninvasive. Expression from both the suf and isc promoters increased in iron-limiting media and in the presence of hydrogen peroxide. Iron repression of the suf promoter was mediated by Fur, and increased suf expression in iron-limiting media was enhanced by the presence of IscR. Iron repression of the isc promoter was mediated by IscR. Hydrogen peroxide-dependent induction of suf expression, but not isc expression, was mediated by OxyR. Furthermore, IscR was a positive regulator of suf expression in the presence of hydrogen peroxide and a negative regulator of isc expression in the absence of hydrogen peroxide. Expression from the S. flexneri suf and isc promoters increased when Shigella was within Henle cells, and our data suggest that the intracellular signal mediating this increased expression is reduced iron levels.

* Corresponding author. Mailing address: Department of Biology, University of Richmond, Richmond, VA 23173. Phone: (804) 287-6390. Fax: (804) 289-8233. E-mail: lrunyenj{at}richmond.edu

{triangledown} Published ahead of print on 14 January 2008.

Editor: J. B. Bliska

Infection and Immunity, March 2008, p. 1083-1092, Vol. 76, No. 3
0019-9567/08/$08.00+0     doi:10.1128/IAI.01211-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





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