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Infection and Immunity, September 2007, p. 4562-4571, Vol. 75, No. 9
0019-9567/07/$08.00+0 doi:10.1128/IAI.00392-07
Copyright © 2007, American Society for Microbiology. 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,1 Institute for Medical Microbiology and Hygiene, University Hospital Tübingen, Tübingen, Germany,2 Institute of Molecular Biology, Center of Excellence for Molecular Medicine, Slovak Academy of Sciences, Bratislava, Slovak Republic,3 Institute of Medical Microbiology and Hygiene, University of Saarland, Homburg, Germany4
Received 15 March 2007/ Returned for modification 25 May 2007/ Accepted 3 July 2007
The alternative transcription factor
B of Staphylococcus 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 (CP synthesis enzyme A) transcription. Deletion of spoVG had a polar effect on yabJ-spoVG transcription and resulted in a two- to threefold decrease in capA transcription. Interestingly, immunofluorescence showed that CP production was strongly impaired in all three mutants, signaling 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 capA expression 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.
Published ahead of print on 16 July 2007.
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