σ B and SarA independently regulate polysaccharide intercellular adhesin production in Staphylococcus epidermidis

L. D. Handke, S. R. Slater, K. M. Conlon, Sinead T. O'Donnell, M. E. Olson, K. A. Bryant, Mark Edmund Rupp, J. P. O'Gara, Paul D Fey

Research output: Contribution to journalArticle

44 Citations (Scopus)

Abstract

The production of polysaccharide intercellular adhesin (PIA) is an essential process in foreign body infections mediated by Staphylococcus epidermidis. Transcriptional regulation of the icaADBC operon, the genes responsible for production of enzymes that synthesize PIA, is multi-factorial and involves at least SarA and σ B . Transcriptional and promoter fusion studies revealed that the decreased transcription of the icaADBC operon observed in a S. epidermidis 1457 sigB mutant is not mediated through a direct interaction of σ B -RNA polymerase at the icaADBC promoter region but instead through the upregulation of IcaR, a known repressor of icaADBC transcription. Transcriptional analysis of a 1457 sigB-icaR double mutant confirmed that the decreased icaADBC transcript in 1457 sigB is IcaR dependent. Furthermore, primer extension studies suggest that the icaR promoter appears to be σ A dependent, suggesting that σ B indirectly controls icaR transcription through an unknown pathway. In addition, it was confirmed that the loss of SarA results in the loss of icaADBC transcription and PIA production in S. epidermidis. It was further demonstrated, through the over-production of SarA in 1457 sigB, that the loss of sarP1 promoter activity in 1457 sigB has little or no effect on the loss of PIA production in this mutant. Finally, it was demonstrated that PIA production could be restored in both 1457 sigB and 1457 sarA by complementing these mutants with a full-length icaADBC operon controlled by a cadmium-inducible noncognate promoter. It is concluded that σ B and SarA operate independently of each other to regulate PIA production and biofilm development in S. epidermidis.

Original languageEnglish (US)
Pages (from-to)82-91
Number of pages10
JournalCanadian journal of microbiology
Volume53
Issue number1
DOIs
StatePublished - Jan 1 2007

Fingerprint

Iron-Dextran Complex
Staphylococcus epidermidis
Operon
RNA Polymerase II
Biofilms
Foreign Bodies
Cadmium
Genetic Promoter Regions
polysaccharide intercellular adhesin
Up-Regulation
Enzymes
Infection
Genes

Keywords

  • Biofilm
  • SarA
  • Staphylococcus epidermidis
  • icaADBC
  • σ

ASJC Scopus subject areas

  • Microbiology
  • Immunology
  • Applied Microbiology and Biotechnology
  • Molecular Biology
  • Genetics

Cite this

σ B and SarA independently regulate polysaccharide intercellular adhesin production in Staphylococcus epidermidis . / Handke, L. D.; Slater, S. R.; Conlon, K. M.; O'Donnell, Sinead T.; Olson, M. E.; Bryant, K. A.; Rupp, Mark Edmund; O'Gara, J. P.; Fey, Paul D.

In: Canadian journal of microbiology, Vol. 53, No. 1, 01.01.2007, p. 82-91.

Research output: Contribution to journalArticle

Handke, L. D. ; Slater, S. R. ; Conlon, K. M. ; O'Donnell, Sinead T. ; Olson, M. E. ; Bryant, K. A. ; Rupp, Mark Edmund ; O'Gara, J. P. ; Fey, Paul D. / σ B and SarA independently regulate polysaccharide intercellular adhesin production in Staphylococcus epidermidis In: Canadian journal of microbiology. 2007 ; Vol. 53, No. 1. pp. 82-91.
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AU - Slater, S. R.

AU - Conlon, K. M.

AU - O'Donnell, Sinead T.

AU - Olson, M. E.

AU - Bryant, K. A.

AU - Rupp, Mark Edmund

AU - O'Gara, J. P.

AU - Fey, Paul D

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N2 - The production of polysaccharide intercellular adhesin (PIA) is an essential process in foreign body infections mediated by Staphylococcus epidermidis. Transcriptional regulation of the icaADBC operon, the genes responsible for production of enzymes that synthesize PIA, is multi-factorial and involves at least SarA and σ B . Transcriptional and promoter fusion studies revealed that the decreased transcription of the icaADBC operon observed in a S. epidermidis 1457 sigB mutant is not mediated through a direct interaction of σ B -RNA polymerase at the icaADBC promoter region but instead through the upregulation of IcaR, a known repressor of icaADBC transcription. Transcriptional analysis of a 1457 sigB-icaR double mutant confirmed that the decreased icaADBC transcript in 1457 sigB is IcaR dependent. Furthermore, primer extension studies suggest that the icaR promoter appears to be σ A dependent, suggesting that σ B indirectly controls icaR transcription through an unknown pathway. In addition, it was confirmed that the loss of SarA results in the loss of icaADBC transcription and PIA production in S. epidermidis. It was further demonstrated, through the over-production of SarA in 1457 sigB, that the loss of sarP1 promoter activity in 1457 sigB has little or no effect on the loss of PIA production in this mutant. Finally, it was demonstrated that PIA production could be restored in both 1457 sigB and 1457 sarA by complementing these mutants with a full-length icaADBC operon controlled by a cadmium-inducible noncognate promoter. It is concluded that σ B and SarA operate independently of each other to regulate PIA production and biofilm development in S. epidermidis.

AB - The production of polysaccharide intercellular adhesin (PIA) is an essential process in foreign body infections mediated by Staphylococcus epidermidis. Transcriptional regulation of the icaADBC operon, the genes responsible for production of enzymes that synthesize PIA, is multi-factorial and involves at least SarA and σ B . Transcriptional and promoter fusion studies revealed that the decreased transcription of the icaADBC operon observed in a S. epidermidis 1457 sigB mutant is not mediated through a direct interaction of σ B -RNA polymerase at the icaADBC promoter region but instead through the upregulation of IcaR, a known repressor of icaADBC transcription. Transcriptional analysis of a 1457 sigB-icaR double mutant confirmed that the decreased icaADBC transcript in 1457 sigB is IcaR dependent. Furthermore, primer extension studies suggest that the icaR promoter appears to be σ A dependent, suggesting that σ B indirectly controls icaR transcription through an unknown pathway. In addition, it was confirmed that the loss of SarA results in the loss of icaADBC transcription and PIA production in S. epidermidis. It was further demonstrated, through the over-production of SarA in 1457 sigB, that the loss of sarP1 promoter activity in 1457 sigB has little or no effect on the loss of PIA production in this mutant. Finally, it was demonstrated that PIA production could be restored in both 1457 sigB and 1457 sarA by complementing these mutants with a full-length icaADBC operon controlled by a cadmium-inducible noncognate promoter. It is concluded that σ B and SarA operate independently of each other to regulate PIA production and biofilm development in S. epidermidis.

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