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Generation and surface localization of intact M protein in Streptococcus pyogenes are dependent on sagA

I Biswas1, P Germon, K McDade

  • 1Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, Georgia 30322, USA.

Infection and Immunity
|October 13, 2001
PubMed

Insights

The sagA gene is crucial for Streptococcus pyogenes M protein surface localization, not its transcription. A mutation in sagA results in truncated M protein, increasing susceptibility to phagocytosis.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Immunology

Background:

  • Streptococcus pyogenes (GAS) M protein is a key surface virulence factor.
  • M protein expression is regulated by the Mga transcriptional activator.
  • The sag locus, involved in streptolysin S production, was hypothesized to regulate M protein transcription.

Purpose of the Study:

  • To investigate the role of the sag locus, specifically sagA, in M protein regulation.
  • To determine if sagA affects M protein gene (emm) transcription or surface localization.

Main Methods:

  • Constructed a sagA insertion-deletion mutant (JRS470) in GAS strain JRS4.
  • Assessed streptolysin S production and M protein levels via cell aggregation and Western blot.
  • Analyzed M protein transcription, structure, and localization using antibodies and Western blot.
  • Evaluated phagocytosis susceptibility of the sagA mutant.

Main Results:

  • The sagA mutant produced no streptolysin S and showed reduced cell surface M protein.
  • emm gene transcription was unaffected by the sagA mutation.
  • M protein in the sagA mutant was truncated, lacking the C-repeat and anchoring domains, and secreted into the supernatant.
  • The sagA mutant lacking surface M protein was susceptible to phagocytosis.

Conclusions:

  • The sagA gene is essential for the proper surface localization and anchoring of M protein in Streptococcus pyogenes.
  • sagA does not regulate emm gene transcription but is critical for post-translational modification or trafficking of M protein.
  • Disruption of M protein surface localization compromises GAS virulence by increasing susceptibility to phagocytosis.

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