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Journal of Bacteriology, November 2003, p. 6640-6647, Vol. 185, No. 22
0021-9193/03/$08.00+0     DOI: 10.1128/JB.185.22.6640-6647.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

MgrA, an Orthologue of Mga, Acts as a Transcriptional Repressor of the Genes within the rlrA Pathogenicity Islet in Streptococcus pneumoniae

Carolyn Hemsley,1 Elizabeth Joyce,2 David L. Hava,3 Amita Kawale,2 and Andrew Camilli3*

Department of Infectious Diseases, Imperial College, London, United Kingdom,1 Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California 94305-5402,2 Department of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, Massachusetts 021113

Received 27 May 2003/ Accepted 21 August 2003

Streptococcus pneumoniae normally resides in the human nasopharynx in a nondisease state. In response to unknown triggers this organism can descend to the lower respiratory tract and/or invade the bloodstream. Regulation and activation of virulence genes play essential roles in this process of disease development. Characterization of S. pneumoniae regulatory networks has been a recent area of interest, but despite inroads little is known about regulation of virulence genes in this pathogen. A putative transcriptional regulator in S. pneumoniae, mgrA, which exhibits homology to the virulence gene activator mga of group A streptococcus, was previously identified as a regulator that is required for development of pneumonia in a murine model. In this study we confirmed that mgrA plays a role in both nasopharyngeal carriage and pneumonia. Transcriptional profiling by microarray technology was used to show that mgrA acts as a repressor of the previously characterized rlrA pathogenicity islet. This is manifested phenotypically by a decrease in adherence to epithelial cells in tissue culture since the rlrA pathogenicity islet contains genes mediating adherence.

* Corresponding author. Mailing address: Department of Molecular Biology and Microbiology, Tufts University School of Medicine, 136 Harrison Avenue, Boston, MA 02111. Phone: (617) 636-2144. Fax: (617) 636-0337. E-mail: Andrew.camilli{at}tufts.edu.

Journal of Bacteriology, November 2003, p. 6640-6647, Vol. 185, No. 22
0021-9193/03/$08.00+0     DOI: 10.1128/JB.185.22.6640-6647.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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