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Regulation of plasmid virulence gene expression in Salmonella dublin involves an unusual operon structure.

TitleRegulation of plasmid virulence gene expression in Salmonella dublin involves an unusual operon structure.
Publication TypeJournal Article
Year of Publication1992
AuthorsKrause, M, Fang, FC, Guiney, DG
JournalJ Bacteriol
Volume174
Issue13
Pagination4482-9
Date Published1992 Jul
ISSN0021-9193
KeywordsBase Sequence, beta-Galactosidase, Blotting, Northern, Codon, Gene Expression Regulation, Bacterial, Genes, Bacterial, Molecular Sequence Data, Oligodeoxyribonucleotides, Operon, Plasmids, Recombinant Fusion Proteins, RNA, Bacterial, RNA, Messenger, Salmonella, Salmonella typhimurium, Species Specificity, Transcription, Genetic, Virulence
Abstract

The 80-kb plasmid pSDL2 of Salmonella dublin Lane is essential for lethal systemic infection in experimental mice. A cluster of five plasmid genes, designated spvR, spvA, spvB, spvC, and spvD, is sufficient to express the plasmid-related virulent phenotype. The spvR gene product has recently been identified as a positive regulator of spvB expression in the stationary phase of bacterial growth (F. C. Fang, M. Krause, C. Roudier, J. Fierer, and D. G. Guiney, J. Bacteriol. 173:6783-6789, 1991). In this study, we evaluated the role of SpvR in the transcription of the downstream virulence genes spvABCD. Analysis of mRNA synthesis revealed that SpvR promotes transcription of the downstream spvABCD genes in the stationary growth phase. Transcript mapping of the spv region demonstrated an unusual operon structure involving messages for spvA, spvAB, spvABC, and spvABCD. Quantitative measurement of transcription and of gene expression by use of translational spv-lacZ fusions suggested that SpvA, SpvB, SpvC, and SpvD are produced in decreasing abundance. Primer extension assays identified two transcriptional start sites 70 and 98 bp upstream of the start codon of spvA, but none upstream of spvB, spvC, or spvD. Deletion of a 320-bp EcoRI-ApaI segment that contains both start sites abolished expression of the downstream spvB and spvC genes. Our results establish a central function of SpvR as a positive regulator of the downstream spvABCD genes in the stationary phase of bacterial growth and indicate that the primary mechanism of regulation is by activation of promoters upstream of spvA.

Alternate JournalJ. Bacteriol.
PubMed ID1378053
PubMed Central IDPMC206235
Grant ListAM35108 / AM / NIADDK NIH HHS / United States
DK01408-05 / DK / NIDDK NIH HHS / United States