This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Sharma, V K Articles by Archer, G L Search for Related Content PubMed PubMed Citation Articles by Sharma, V K Articles by Archer, G L

Next Article 

J Bacteriol. 1994 June; 176(12): 3445-3454

research-article

Transcriptional regulation by TrsN of conjugative transfer genes on staphylococcal plasmid pGO1.

Department of Medicine, Medical College of Virginia, Virginia Commonwealth University, Richmond 23298-0049.

ABSTRACT

The major conjugative transfer gene cluster of staphylococcal plasmid pGO1 (trs) consists of 13 open reading frames (trsA to trsM) transcribed from one DNA strand and a single 189-bp open reading frame (trsN) within the first 348 bp of trs that is transcribed divergently. Promoter regions for trsN and trsA partially overlap. TrsN, a 7,181-Da protein, was purified as a fusion to glutathione S-transferase and found to have DNA-binding activity. Increasing concentrations of the fusion protein progressively retarded the gel migration of PCR-generated DNA fragments containing predicted promoters 5' to trsL, trsA, and trsN. The target sequences contained areas of identity, including regions of dyad symmetry, that were protected in DNase I footprinting studies. The binding of TrsN to its trsL target was required for this target DNA to be stably introduced into Staphylococcus aureus on a high-copy-number vector. Provision of excess TrsN from this high-copy-number vector in S. aureus decreased beta-galactosidase activity from a trsL-lacZ transcriptional fusion and decreased pGO1 conjugation frequency. Conversely, both transcription and conjugation increased in the presence of excess trsL target. We propose that TrsN negatively regulates the transcription of genes essential for conjugative transfer by binding to regions 5' to their translational start sites.

This article has been cited by other articles:

• Grohmann, E., Muth, G., Espinosa, M. (2003). Conjugative Plasmid Transfer in Gram-Positive Bacteria. Microbiol. Mol. Biol. Rev. 67: 277-301 [Abstract] [Full Text]  
• Dickinson, T. M., Archer, G. L. (2000). Phenotypic Expression of Oxacillin Resistance in Staphylococcus epidermidis: Roles of mecA Transcriptional Regulation and Resistant-Subpopulation Selection. Antimicrob. Agents Chemother. 44: 1616-1623 [Abstract] [Full Text]  
• Berg, T., Firth, N., Apisiridej, S., Hettiaratchi, A., Leelaporn, A., Skurray, R. A. (1998). Complete Nucleotide Sequence of pSK41: Evolution of Staphylococcal Conjugative Multiresistance Plasmids. J. Bacteriol. 180: 4350-4359 [Abstract] [Full Text]  
• Sharma, V. K., Hackbarth, C. J., Dickinson, T. M., Archer, G. L. (1998). Interaction of Native and Mutant MecI Repressors with Sequences That Regulate mecA, the Gene Encoding Penicillin Binding Protein 2a in Methicillin-Resistant Staphylococci. J. Bacteriol. 180: 2160-2166 [Abstract] [Full Text]