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Journal of Bacteriology, August 2005, p. 5658-5664, Vol. 187, No. 16
0021-9193/05/$08.00+0     doi:10.1128/JB.187.16.5658-5664.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Shigella dysenteriae ShuS Promotes Utilization of Heme as an Iron Source and Protects against Heme Toxicity

Elizabeth E. Wyckoff,* Gregory F. Lopreato,{dagger} Kimberly A. Tipton,{ddagger} and Shelley M. Payne

Section of Molecular Genetics and Microbiology and Institute of Cellular and Molecular Biology, The University of Texas, Austin, Texas 78712

Received 20 December 2004/ Accepted 19 May 2005

Shigella dysenteriae serotype 1, a major cause of bacillary dysentery in humans, can use heme as a source of iron. Genes for the transport of heme into the bacterial cell have been identified, but little is known about proteins that control the fate of the heme molecule after it has entered the cell. The shuS gene is located within the heme transport locus, downstream of the heme receptor gene shuA. ShuS is a heme binding protein, but its role in heme utilization is poorly understood. In this work, we report the construction of a chromosomal shuS mutant. The shuS mutant was defective in utilizing heme as an iron source. At low heme concentrations, the shuS mutant grew slowly and its growth was stimulated by either increasing the heme concentration or by providing extra copies of the heme receptor shuA on a plasmid. At intermediate heme concentrations, the growth of the shuS mutant was moderately impaired, and at high heme concentrations, shuS was required for growth on heme. The shuS mutant did not show increased sensitivity to hydrogen peroxide, even at high heme concentrations. ShuS was also required for optimal utilization of heme under microaerobic and anaerobic conditions. These data are consistent with the model in which ShuS binds heme in a soluble, nontoxic form and potentially transfers the heme from the transport proteins in the membrane to either heme-containing or heme-degrading proteins. ShuS did not appear to store heme for future use.


* Corresponding author. Mailing address: The University of Texas, Section of Molecular Genetics and Microbiology, 1 University Station A5000, Austin, TX 78712-0162. Phone: (512) 471-5204. Fax: (512) 471-7088. E-mail: ewyckoff{at}mail.utexas.edu.

{dagger} Present address: GeneXpress Informatics, 13091 Pond Springs Rd., Suite 150, Austin, TX 78729.

{ddagger} Present address: Howard Hughes Medical Institute, Department of Cellular and Molecular Pharmacology, and Department of Biochemistry and Biophysics, University of California—San Francisco, 600 16th Street, San Francisco, CA 94143-2240.


Journal of Bacteriology, August 2005, p. 5658-5664, Vol. 187, No. 16
0021-9193/05/$08.00+0     doi:10.1128/JB.187.16.5658-5664.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.




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