Regulation of biofilm formation by sigma B is a common mechanism in Staphylococcus epidermidis and is not mediated by transcriptional regulation of sarA.
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Regulation of biofilm formation by sigma B is a common mechanism in Staphylococcus epidermidis and is not mediated by transcriptional regulation of sarA. / Jäger, Sebastian; Jonas, Beate; Pfanzelt, Dorothea; Horstkotte, Matthias A; Rohde, Holger; Mack, Dietrich; Knobloch, Johannes K-M.
In: INT J ARTIF ORGANS, Vol. 32, No. 9, 9, 2009, p. 584-591.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Regulation of biofilm formation by sigma B is a common mechanism in Staphylococcus epidermidis and is not mediated by transcriptional regulation of sarA.
AU - Jäger, Sebastian
AU - Jonas, Beate
AU - Pfanzelt, Dorothea
AU - Horstkotte, Matthias A
AU - Rohde, Holger
AU - Mack, Dietrich
AU - Knobloch, Johannes K-M
PY - 2009
Y1 - 2009
N2 - 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.
AB - 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.
U2 - 10.1177/039139880903200907
DO - 10.1177/039139880903200907
M3 - SCORING: Zeitschriftenaufsatz
VL - 32
SP - 584
EP - 591
JO - INT J ARTIF ORGANS
JF - INT J ARTIF ORGANS
SN - 0391-3988
IS - 9
M1 - 9
ER -