Affiliation:
1. Department of Cell Biology, Microbiology & Molecular Biology, University of South Florida, Tampa, Florida, USA
Abstract
ABSTRACT
Previously we identified a novel component of the
Staphylococcus aureus
regulatory network, an
e
xtra
c
ytoplasmic
f
unction σ-factor, σ
S
, involved in stress response and disease causation. Here we present additional characterization of σ
S
, demonstrating a role for it in protection against DNA damage, cell wall disruption, and interaction with components of the innate immune system. Promoter mapping reveals the existence of three unique
sigS
start sites, one of which appears to be subject to autoregulation. Transcriptional profiling revealed that
sigS
expression remains low in a number of
S. aureus
wild types but is upregulated in the highly mutated strain RN4220. Further analysis demonstrates that
sigS
expression is inducible upon exposure to a variety of chemical stressors that elicit DNA damage, including methyl methanesulfonate and ciprofloxacin, as well as those that disrupt cell wall stability, such as ampicillin and oxacillin. Significantly, expression of
sigS
is highly induced during growth in serum and upon phagocytosis by RAW 264.7 murine macrophage-like cells. Phenotypically, σ
S
mutants display sensitivity to a broad range of DNA-damaging agents and cell wall-targeting antibiotics. Furthermore, the survivability of σ
S
mutants is strongly impacted during challenge by components of the innate immune system. Collectively, our data suggest that σ
S
likely serves dual functions within the
S. aureus
cell, protecting against both cytoplasmic and extracytoplasmic stresses. This further argues for its important, and perhaps novel, role in the
S. aureus
stress and virulence responses.
Publisher
American Society for Microbiology
Subject
Molecular Biology,Microbiology
Cited by
42 articles.
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