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Related Experiment Video

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Protocols for Robust Herbicide Resistance Testing in Different Weed Species

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Published on: July 2, 2015

svrA, a multi-drug exporter, does not control agr.

John Chen¹, Richard P Novick¹

¹Program in Molecular Pathogenesis, Skirball Institute, and Departments of Microbiology and Medicine, New York University Medical Center, New York 10016, USA.

Microbiology (Reading, England)

|April 28, 2007

Summary

The Staphylococcus aureus svrA gene does not impact virulence through the agr pathway. Further research confirmed svrA is not involved in agr activation or Staphylococcus aureus infections.

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Area of Science:

Microbiology
Bacterial Pathogenesis
Molecular Biology

Background:

The Staphylococcus aureus svrA gene was initially identified in a screen for mutations affecting mouse virulence.
This gene was found to be defective in accessory gene regulator (agr) expression, a key virulence factor in S. aureus.

Purpose of the Study:

To investigate the role of the svrA gene in Staphylococcus aureus virulence.
To determine if svrA influences virulence through the agr regulatory system.

Main Methods:

Signature-tagged mutagenesis using Tn917 was employed to identify attenuated S. aureus mutants.
The svrA mutation was separated from an adventitious agrC frame-shift mutation in the original strain.
Agr activation was assessed by analyzing exoprotein profiles and haemolytic toxin production.

Main Results:

The svrA gene itself was found to have no detectable effect on agr activation.
Separating the svrA mutation from the agrC mutation demonstrated svrA does not influence exoprotein profiles or haemolytic toxin production.
The original mutant strain's virulence defect was primarily due to the agrC mutation.

Conclusions:

The svrA gene does not play a role in Staphylococcus aureus infections via an agr-mediated pathway.
The previously observed attenuation of virulence in svrA mutants was likely due to a linked agrC mutation.