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Redox sensing by a Rex-family repressor is involved in the regulation of anaerobic gene expression in Staphylococcus aureus

In English

Författare

  • Martin Pagels
  • Stephan Fuchs
  • Jan Pane-Farre
  • Christian Kohler
  • Leonhard Menschner
  • Michael Hecker
  • Peter J. McNamarra
  • Mikael Bauer
  • Claes von Wachenfeldt
  • Manuel Liebeke
  • Michael Lalk
  • Gunnar Sander
  • Christof von Eiff
  • Richard A. Proctor
  • Susanne Engelmann
Visa allt

Summary, in English

P>An alignment of upstream regions of anaerobically induced genes in Staphylococcus aureus revealed the presence of an inverted repeat, corresponding to Rex binding sites in Streptomyces coelicolor. Gel shift experiments of selected upstream regions demonstrated that the redox-sensing regulator Rex of S. aureus binds to this inverted repeat. The binding sequence - TTGTGAAW(4)TTCACAA - is highly conserved in S. aureus. Rex binding to this sequence leads to the repression of genes located downstream. The binding activity of Rex is enhanced by NAD+ while NADH, which competes with NAD+ for Rex binding, decreases the activity of Rex. The impact of Rex on global protein synthesis and on the activity of fermentation pathways under aerobic and anaerobic conditions was analysed by using a rex-deficient strain. A direct regulatory effect of Rex on the expression of pathways that lead to anaerobic NAD+ regeneration, such as lactate, formate and ethanol formation, nitrate respiration, and ATP synthesis, is verified. Rex can be considered a central regulator of anaerobic metabolism in S. aureus. Since the activity of lactate dehydrogenase enables S. aureus to resist NO stress and thus the innate immune response, our data suggest that deactivation of Rex is a prerequisite for this phenomenon.

Publiceringsår

2010

Språk

Engelska

Sidor

1142-1161

Publikation/Tidskrift/Serie

Molecular Microbiology

Volym

76

Issue

5

Dokumenttyp

Artikel i tidskrift

Förlag

Wiley-Blackwell

Ämne

  • Biological Sciences
  • Physical Chemistry

Status

Published

Forskningsgrupp

  • Microbiology Group

ISBN/ISSN/Övrigt

  • ISSN: 1365-2958