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Attenuated expression of the mga virulence regulon in an M serotype 50 mouse-virulent group A streptococcal strain

D L Yung1, K S McIver, J R Scott

  • 1Department of Microbiology, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA.

Infection and Immunity
|November 24, 1999
PubMed

Insights

A defect in the Mga regulator of group A Streptococcus impairs virulence gene expression in mice. Restoring Mga function via gene complementation re-established virulence.

Area of Science:

  • Microbiology
  • Bacterial genetics
  • Streptococcal infections

Background:

  • Group A Streptococcus (GAS) causes various infections.
  • Virulence gene expression is crucial for GAS pathogenesis.
  • The Mga regulator controls multiple GAS virulence factors.

Purpose of the Study:

  • To investigate the role of a defective Mga regulator in GAS virulence.
  • To identify specific mutations within the mga gene.
  • To restore GAS virulence by complementing the mga defect.

Main Methods:

  • Sequencing the mga gene to identify mutations.
  • Allelic exchange to introduce mga alleles.
  • Quantitative reverse transcription-PCR to measure emm50 transcript levels.
  • Western blotting or ELISA to quantify M protein.

Main Results:

  • A GAS strain with attenuated virulence showed three amino acid changes in Mga.
  • Complementation with wild-type or divergent mga alleles restored Mga function.
  • emm50 transcript levels and surface M protein quantity increased after complementation.

Conclusions:

  • A defective Mga regulator is responsible for reduced virulence gene expression in this GAS strain.
  • Restoring Mga function through genetic complementation re-establishes virulence.
  • Mga is essential for regulating GAS virulence in a mouse model.

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