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Infection and Immunity, September 2005, p. 5995-6004, Vol. 73, No. 9
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.9.5995-6004.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Bordetella pertussis risA, but Not risS, Is Required for Maximal Expression of Bvg-Repressed Genes

Trevor H. Stenson,1* Andrew G. Allen,2,{dagger} Jehan A. al-Meer,2,{ddagger} Duncan Maskell,2,§ and Mark S. Peppler1

Department of Medical Microbiology and Immunology, University of Alberta, 1-69 Medical Sciences Bldg., Edmonton, Alberta T6G 2H7, Canada,1 Department of Biochemistry, Imperial College of Science, Technology and Medicine, London SW7 2AZ, United Kingdom2

Received 11 January 2005/ Returned for modification 29 March 2005/ Accepted 26 April 2005

Expression of virulence determinants by Bordetella pertussis, the primary etiological agent of whooping cough, is regulated by the BvgAS two-component regulatory system. The role of a second two-component regulatory system, encoded by risAS, in this process is not defined. Here, we show that mutation of B. pertussis risA does not affect Bvg-activated genes or proteins. However, mutation of risA resulted in greatly diminished expression of Bvg-repressed antigens and decreased transcription of Bvg-repressed genes. In contrast, mutation of risS had no effect on the expression of Bvg-regulated molecules. Mutation of risA also resulted in decreased bacterial invasion in a HeLa cell model. However, decreased invasion could not be attributed to the decreased expression of Bvg-repressed products, suggesting that mutation of risA may affect the expression of a variety of genes. Unlike the risAS operons in B. parapertussis and B. bronchiseptica, B. pertussis risS is a pseudogene that encodes a truncated RisS sensor. Deletion of the intact part of the B. pertussis risS gene does not affect the expression of risA-dependent, Bvg-repressed genes. These observations suggest that RisA activation occurs through cross-regulation by a heterologous system.

* Corresponding author. Mailing address: Department of Medical Microbiology and Immunology, University of Alberta, 1-69 Medical Sciences Bldg., Edmonton, Alberta T6G 2H7, Canada. Phone: (780) 492-0934. Fax: (780) 492-7521. E-mail: trevor.stenson{at}ualberta.ca.

Editor: V. J. DiRita

{dagger} Present address: Oxford Gene Technology IP Ltd., Begbroke Business & Science Park, Sandy Lane, Yarnton, Oxford OX5 1PF, United Kingdom.

{ddagger} Present address: University of Qatar, Faculty of Science, Chemistry and Biochemistry Department, P.O. Box 2713, Doha, Qatar.

§ Present address: The Centre for Veterinary Science, Department of Veterinary Medicine, University of Cambridge, Madingley Road, Cambridge CB3 0ES, United Kingdom.

Infection and Immunity, September 2005, p. 5995-6004, Vol. 73, No. 9
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.9.5995-6004.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.





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