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SarT, a repressor of alpha-hemolysin in Staphylococcus aureus
K A Schmidt1, A C Manna, S Gill
1Department of Microbiology, Dartmouth Medical School, Hanover, New Hampshire 13755, USA. Katherine.a.schmidt@dartmouth.edu
Infection and Immunity
|July 12, 2001
Summary
Staphylococcus aureus SarA protein induces alpha-hemolysin by repressing sarT. SarT normally inhibits alpha-hemolysin production, but SarA
Area of Science:
- Microbiology
- Molecular Biology
- Genetics
Background:
- Staphylococcus aureus utilizes complex regulatory networks for virulence factor production.
- SarA and Agr are key regulators of virulence gene expression in S. aureus.
Purpose of the Study:
- To investigate the role of a novel SarA homolog, sarT, in regulating Staphylococcus aureus virulence.
- To elucidate the regulatory relationship between sarA, agr, and sarT in alpha-hemolysin (hla) expression.
Main Methods:
- Genome searching for SarA homologs.
- Northern blot and Western blot analyses for gene and protein expression.
- Insertion mutagenesis to create sarT mutants.
- Rabbit erythrocyte hemolytic assay for alpha-hemolysin activity.
- Complementation studies.
Main Results:
- Identified sarT, encoding a 118-residue protein, repressed by sarA and agr.
- SarT represses alpha-hemolysin (hla) expression.
- A sarT mutation increased RNAIII levels and relieved hla repression.
- SarA induced hla by repressing sarT, while agr repressed hla.
Conclusions:
- SarA positively regulates alpha-hemolysin production through repression of the sarT repressor.
- SarT acts as a repressor of hla transcription in Staphylococcus aureus.
- The interplay between SarA, Agr, and SarT highlights intricate virulence regulation in S. aureus.