Previous Article | Next Article ![]()
Journal of Bacteriology, November 2006, p. 7626-7634, Vol. 188, No. 21
0021-9193/06/$08.00+0 doi:10.1128/JB.01059-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
Veterans Affairs Medical Center, Infectious Diseases Section, Boise, Idaho,1 University of Idaho, Moscow, Idaho,2 Department of Microbiology, Molecular Biology, and Biochemistry, University of Washington School of Medicine, Seattle, Washington3
Received 19 July 2006/ Accepted 23 August 2006
Severe, invasive group A streptococcal infections have reemerged worldwide, and extracellular toxins, including streptococcal pyrogenic exotoxin B (SpeB), have been implicated in pathogenesis. The genetic regulation of SpeB is not fully understood, and the mechanisms involved in the processing of the protoxin to its enzymatically active form have not been definitively established. The present work demonstrated that the genes encoding SpeB (speB) and a peptidyl-prolyl isomerase (prsA) constitute an operon with transcription initiated from two promoters upstream of speB. Further, the speB-prsA operon was transcribed as a bicistronic mRNA. This finding is in contrast to the generally accepted notion that speB is transcribed only as a monocistronic gene. In addition, prsA has its own promoter, and transcription from this promoter starts in early log phase, prior to the transcription of speB. Genomic disruption of prsA decreased the production of enzymatically active SpeB but not the level of the pro-SpeB zymogen. Taken together, these results demonstrate that prsA is required for production of fully mature, enzymatically active SpeB.
Published ahead of print on 1 September 2006.
This article has been cited by other articles:
Copyright © 2009 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»