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Strain-specific impact of PsaR of Streptococcus pneumoniae on global gene expression and virulence

Wouter T Hendriksen1, Hester J Bootsma2, Angela van Diepen2

  • 1Department of Pediatrics, Erasmus MC-Sophia Children's Hospital, 3000 DR Rotterdam, The Netherlands.

Microbiology (Reading, England)
|April 18, 2009
PubMed

Insights

The PsaR regulator in Streptococcus pneumoniae influences gene expression differently between strains D39 and TIGR4. This study reveals strain-specific roles for PsaR in bacterial virulence and infection development.

Area of Science:

  • Microbiology
  • Genetics
  • Infectious Diseases

Background:

  • PsaR is a known manganese-dependent regulator in Streptococcus pneumoniae, previously shown to negatively regulate at least seven genes.
  • Understanding the full regulatory role of PsaR is crucial for deciphering Streptococcus pneumoniae pathogenesis.

Purpose of the Study:

  • To comprehensively analyze the global gene expression targets of PsaR in Streptococcus pneumoniae strains D39 and TIGR4 using transcriptome and proteome analysis.
  • To investigate the contribution of PsaR to Streptococcus pneumoniae virulence in murine infection models.

Main Methods:

  • Transcriptome analysis (microarray) and proteome analysis were performed on wild-type and psaR mutant strains (D39 and TIGR4).
  • Comparative analysis of PsaR-regulated genes was conducted between the two strains.
  • Murine infection models (colonization, pneumonia, and bacteraemia) were used to assess the in vivo virulence of wild-type and psaR mutant strains.

Main Results:

  • Shared PsaR targets included the psa operon, pcpA, and prtA. Strain D39 showed unique regulation of a cellobiose-specific phosphotransferase system (PTS) and a bacteriocin operon.
  • Strain TIGR4 exhibited unique regulation of the rlrA pathogenicity islet.
  • PsaR demonstrated strain-specific effects on virulence; D39 psaR mutants showed initial survival advantage in pneumonia and reduced bacteraemia, while TIGR4 psaR mutants showed reduced bacterial load in pneumonia at 24h and attenuation in bacteraemia at 36h.

Conclusions:

  • PsaR exhibits a strain-specific regulatory role in global gene expression in Streptococcus pneumoniae.
  • The PsaR regulator plays a differential role in the development of bacteraemia and virulence depending on the bacterial strain.

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