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Infect. Immun. doi:10.1128/IAI.00392-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

^B and the ^B-dependent arlRS and yabJ-spoVG loci affect capsule formation in Staphylococcus aureus

Institute of Medical Microbiology, University of Zürich, Zürich, Switzerland, Institute for Medical Microbiology and Hygiene, University Hospital Tübingen, Tübingen, Germany, Institute of Molecular Biology, Centre of Excellence for Molecular Medicine, Slovak Academy of Sciences, Bratislava, Slovak Republic, Institute of Medical Microbiology and Hygiene, University of Saarland, Homburg, Germany

^* To whom correspondence should be addressed. Email: Bischoff{at}immv.uzh.ch.

	Abstract

The alternative transcription factor ^B of Staphylcococcus aureus affects the transcription of the cap gene cluster, required for the synthesis of capsular polysaccharide (CP), although this operon is lacking an apparent ^B-dependent promoter. Regulation of cap expression and CP production in S. aureus strain Newman was shown here to be influenced by ^B, the two-component signal transduction regulatory system ArlRS, and the yabJ-spoVG locus to different extents. Inactivation of arlR or deletion of the sigB operon strongly suppressed capA (capsular polysaccharide synthesis enzyme A) transcription. Deletion of spoVG had a polar effect on yabJ-spoVG transcription and resulted in a two to three-fold decrease of capA transcription. Interestingly, immunofluorescence showed that capsule polysaccharide production was strongly impaired in all three mutants, signalling that the yabJ-spoVG inactivation, despite its only partial effect on capA transcription, abolished capsule formation. Trans-complementation of the spoVG mutant with yabJ-spoVG under the control of its native promoter restored CP-5 production and the capA expression level to levels seen in the wild-type. Northern analyses revealed a strong impact of ^B on arlRS and yabJ-spoVG transcription. We hypothesize that ArlR and products of the yabJ-spoVG locus may serve as effectors that modulate ^B control over ^B-dependent genes lacking an apparent ^B promoter.