JB Accepts, published online ahead of print on 1 September 2006

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J. Bacteriol. doi:10.1128/JB.01059-06
Copyright (c) 2006, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Identification and characterization of bicistronic speB and prsA gene expression in Group A Streptococcus

Yongsheng Ma^*, Amy E. Bryant, Dan B. Salmi, Susan M. Hayes-Schroer, Eric McIndoo, Michael J. Aldape, and Dennis L. Stevens

Veterans Affairs Medical Center, Infectious Diseases Section, Boise, ID; University of Idaho, Moscow, ID; University of Washington School of Medicine, Seattle, WA

^* To whom correspondence should be addressed. Email: yongsheng.ma{at}va.gov.,

Severe invasive group A streptococcal infections (GAS) have re-emerged 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 only transcribed as a monocistronic gene. In addition, prsA has its own promoter and transcription from this promoter starts in early log phase prior to 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 prsA is required for production of fully mature, enzymatically active, SpeB.

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