Dataset Information

Sigma(B) activity depends on RsbU in Staphylococcus aureus.

ABSTRACT: Derivatives of the widely used laboratory strain Staphylococcus aureus NCTC8325, which are natural rsbU mutants, were shown to be unable to produce RsbU, a positive regulator of the alternative sigma factor sigma(B). The lack of RsbU prevented the heat-dependent production of sigma(B)-controlled transcripts and resulted in reduced H2O2 and UV tolerance, enhanced alpha-hemolysin activity, and the inability to produce the alkaline shock protein Asp23. After 48 h of growth, rsbU mutant strains failed to accumulate staphyloxanthin, the major stationary-phase carotenoid. Transcription of Asp23 was found to be exclusively controlled by sigma(B), making it an excellent target for the study of sigma(B) activity in S. aureus. Reporter gene experiments, using the firefly luciferase gene (luc+) fused to the sigma(B)-dependent promoter(s) of asp23, revealed that sigma(B) is almost inactive in 8325 derivatives. cis complementation of the 8325 derivative BB255 with the wild-type rsbU gene from strain COL produced the rsbU(+) derivative GP268, a strain possessing a sigma(B) activity profile comparable to that of the rsbU(+) wild-type strain Newman. In GP268, the heat inducibility of sigma(B)-dependent genes, Asp23 production, alpha-hemolysin activity, pigmentation, and susceptibility to H2O2 were restored to the levels observed in strain Newman, clearly demonstrating that RsbU is needed for activation of sigma(B) in S. aureus.

SUBMITTER: Giachino P

PROVIDER: S-EPMC95078 | biostudies-literature | 2001 Mar

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Sigma(B) activity depends on RsbU in Staphylococcus aureus.

Giachino P P Engelmann S S Bischoff M M

Journal of bacteriology 20010301 6

Derivatives of the widely used laboratory strain Staphylococcus aureus NCTC8325, which are natural rsbU mutants, were shown to be unable to produce RsbU, a positive regulator of the alternative sigma factor sigma(B). The lack of RsbU prevented the heat-dependent production of sigma(B)-controlled transcripts and resulted in reduced H2O2 and UV tolerance, enhanced alpha-hemolysin activity, and the inability to produce the alkaline shock protein Asp23. After 48 h of growth, rsbU mutant strains fail ...[more]

PMID: 11222581

Similar Datasets

Project description:Staphylococcus aureus is a major human pathogen that causes a range of infections from acute invasive to chronic and difficult-to-treat. Infection strategies associated with persisting S. aureus infections are bacterial host cell invasion and the bacterial ability to dynamically change phenotypes from the aggressive wild-type to small colony variants (SCVs), which are adapted for intracellular long-term persistence. The underlying mechanisms of the bacterial switching and adaptation mechanisms appear to be very dynamic, but are largely unknown. Here, we analyzed the role and the crosstalk of the global S. aureus regulators agr, sarA and SigB by generating single, double and triple mutants, and testing them with proteome analysis and in different in vitro and in vivo infection models. We were able to demonstrate that SigB is the crucial factor for adaptation in chronic infections. During acute infection, the bacteria require the simultaneous action of the agr and sarA loci to defend against invading immune cells by causing inflammation and cytotoxicity and to escape from phagosomes in their host cells that enable them to settle an infection at high bacterial density. To persist intracellularly the bacteria subsequently need to silence agr and sarA. Indeed agr and sarA deletion mutants expressed a much lower number of virulence factors and could persist at high numbers intracellularly. SigB plays a crucial function to promote bacterial intracellular persistence. In fact, ?sigB-mutants did not generate SCVs and were completely cleared by the host cells within a few days. In this study we identified SigB as an essential factor that enables the bacteria to switch from the highly aggressive phenotype that settles an acute infection to a silent SCV-phenotype that allows for long-term intracellular persistence. Consequently, the SigB-operon represents a possible target to develop preventive and therapeutic strategies against chronic and therapy-refractory infections.

Dataset Information

Sigma(B) activity depends on RsbU in Staphylococcus aureus.

Publications

Sigma(B) activity depends on RsbU in Staphylococcus aureus.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets