This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Puri-Taneja, A.
Right arrow Articles by Hulett, F. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Puri-Taneja, A.
Right arrow Articles by Hulett, F. M.

 Previous Article  |  Next Article 

Journal of Bacteriology, February 2006, p. 1266-1278, Vol. 188, No. 4
0021-9193/06/$08.00+0     doi:10.1128/JB.188.4.1266-1278.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

CcpA Causes Repression of the phoPR Promoter through a Novel Transcription Start Site, PA6

Ankita Puri-Taneja, Salbi Paul, Yinghua Chen,{dagger} and F. Marion Hulett*

Laboratory for Molecular Biology, Department of Biological Sciences, University of Illinois at Chicago, Chicago, Illinois 60607

Received 25 August 2005/ Accepted 23 November 2005

The Bacillus subtilis PhoPR two-component system is directly responsible for activation or repression of Pho regulon genes in response to phosphate deprivation. The response regulator, PhoP, and the histidine kinase, PhoR, are encoded in a single operon with a complex promoter region that contains five known transcription start sites, which respond to at least two regulatory proteins. We report here the identification of another direct regulator of phoPR transcription, carbon catabolite protein A, CcpA. This regulator functions in the presence of glucose or other readily metabolized carbon sources. The maximum derepression of phoPR expression in a ccpA mutant compared to a wild-type stain was observed under excess phosphate conditions with glucose either throughout growth in a high-phosphate defined medium or in a low-phosphate defined medium during exponential growth, a growth condition when phoPR transcription is low in a wild-type strain due to the absence of autoinduction. Either HPr or Crh were sufficient to cause CcpA dependent repression of the phoPR promoter in vivo. A ptsH1 (Hpr) crh double mutant completely relieves phoPR repression during phosphate starvation but not during phosphate replete growth. In vivo and in vitro studies showed that CcpA repressed phoPR transcription by binding directly to the cre consensus sequence present in the promoter. Primer extension and in vitro transcription studies revealed that the CcpA regulation of phoPR transcription was due to repression of PA6, a previously unidentified promoter positioned immediately upstream of the cre box. E{sigma}A was sufficient for transcription of PA6, which was repressed by CcpA in vitro. These studies showed direct repression by CcpA of a newly discovered E{sigma}A-responsive phoPR promoter that required either Hpr or Crh in vivo for direct binding to the putative consensus cre sequence located between PA6 and the five downstream promoters characterized previously.

* Corresponding author. Mailing address: Laboratory for Molecular Biology, Department of Biological Sciences, University of Illinois at Chicago, 900 S. Ashland Ave. (M/C 567), Chicago, IL 60607. Phone: (312) 996-2280. Fax: (312) 413-2691. E-mail: Hulett{at}uic.edu.

{dagger} Present address: Department of Medicine, Section of Hematology-Oncology, University of Chicago, Chicago, Ill.

Journal of Bacteriology, February 2006, p. 1266-1278, Vol. 188, No. 4
0021-9193/06/$08.00+0     doi:10.1128/JB.188.4.1266-1278.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Rodriguez-Garcia, A., Sola-Landa, A., Apel, K., Santos-Beneit, F., Martin, J. F. (2009). Phosphate control over nitrogen metabolism in Streptomyces coelicolor: direct and indirect negative control of glnR, glnA, glnII and amtB expression by the response regulator PhoP. Nucleic Acids Res 37: 3230-3242 [Abstract] [Full Text]  
  • Santos-Beneit, F., Rodriguez-Garcia, A., Apel, A. K., Martin, J. F. (2009). Phosphate and carbon source regulation of two PhoP-dependent glycerophosphodiester phosphodiesterase genes of Streptomyces coelicolor. Microbiology 155: 1800-1811 [Abstract] [Full Text]  
  • Mendez, M., Huang, I-H., Ohtani, K., Grau, R., Shimizu, T., Sarker, M. R. (2008). Carbon Catabolite Repression of Type IV Pilus-Dependent Gliding Motility in the Anaerobic Pathogen Clostridium perfringens. J. Bacteriol. 190: 48-60 [Abstract] [Full Text]  
  • Puri-Taneja, A., Schau, M., Chen, Y., Hulett, F. M. (2007). Regulators of the Bacillus subtilis cydABCD Operon: Identification of a Negative Regulator, CcpA, and a Positive Regulator, ResD. J. Bacteriol. 189: 3348-3358 [Abstract] [Full Text]  
  • Makarewicz, O., Dubrac, S., Msadek, T., Borriss, R. (2006). Dual Role of the PhoP~P Response Regulator: Bacillus amyloliquefaciens FZB45 Phytase Gene Transcription Is Directed by Positive and Negative Interactions with the phyC Promoter.. J. Bacteriol. 188: 6953-6965 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»