Regulation of biofilm formation by sigma B is a common mechanism in Staphylococcus epidermidis and is not mediated by transcriptional regulation of sarA.

Standard

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, Jahrgang 32, Nr. 9, 9, 2009, S. 584-591.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

Harvard

APA

Vancouver

Bibtex

@article{d4628c080d644c1b9c58d4b26c67c2a8,
title = "Regulation of biofilm formation by sigma B is a common mechanism in Staphylococcus epidermidis and is not mediated by transcriptional regulation of sarA.",
abstract = "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.",
author = "Sebastian J{\"a}ger and Beate Jonas and Dorothea Pfanzelt and Horstkotte, {Matthias A} and Holger Rohde and Dietrich Mack and Knobloch, {Johannes K-M}",
year = "2009",
doi = "10.1177/039139880903200907",
language = "Deutsch",
volume = "32",
pages = "584--591",
journal = "INT J ARTIF ORGANS",
issn = "0391-3988",
publisher = "Wichtig Publishing",
number = "9",

}

RIS

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 -