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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2009-11-9
pubmed:abstractText
Biofilm formation is a major pathogenetic factor of Staphylococcus epidermidis. In S. epidermidis the alternative sigma factor sigma B was identified to regulate biofilm formation in S. epidermidis 1457. In S. aureus sigma B dependent regulation plays a minor role, whereas sarA (Staphylococcus accessory regulator) is an essential regulator. Therefore, we investigated the impact of sigma B on sarA transcription and biofilm formation in three independent S. epidermidis isolates. Mutants with dysfunctional sigma B displayed a strongly reduced biofilm formation, whereas in mutants with constitutive sigma B activity biofilm formation was increased. Transcriptional analysis revealed that icaA transcription was down-regulated in all sigma B negative mutants while icaR transcription was up-regulated. However, transcriptional differences varied between individual strains, indicating that additional sigma B-dependent regulators are involved in biofilm expression. Interestingly, despite the presence of a sigma B promoter beside two sigma A promoters no differences, or only minor ones, were observed in sarA transcription, indicating that sigma B-dependent sarA transcript has no influence on the phenotypic changes. The data observed in independent clinical S. epidermidis isolates suggests that, in contrast to S. aureus, regulation of biofilm formation by sigma B is a general feature in S. epidermidis. Additionally, we were able to demonstrate that the sarA- dependent regulation is not involved in this regulatory pathway.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0391-3988
pubmed:author
pubmed:issnType
Print
pubmed:volume
32
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
584-91
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Regulation of biofilm formation by sigma B is a common mechanism in Staphylococcus epidermidis and is not mediated by transcriptional regulation of sarA.
pubmed:affiliation
Department of Cardiology and Pneumology, Charité Universitätsmedizin Berlin, Campus Benjamin Franklin, Berlin, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't