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Published online ahead of print on 16 April 2009 as doi:10.1099/mic.0.025072-0
Microbiology 2009;155:1569.

Microbiology (2009), DOI 10.1099/mic.0.025072-0
© 2009 Society for General Microbiology
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Microbiology 0 (2009), mic.0.025072; DOI  10.1099/mic.0.025072-0
© 2009 Society for General Microbiology

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

W. T. Hendriksen1, H. J. Bootsma2, A. van Diepen2, S. Estevão1, O. P. Kuipers3, R. de Groot2 and P. W. M. Hermans2,4

1 Department of Pediatrics, Erasmus MC-Sophia Children's Hospital;
2 Laboratory of Pediatric Infectious Diseases, Radboud University Nijmegen Medical Centre;
3 University of Groningen, Molecular Genetics

ABSTRACT

Previous studies have indicated that PsaR of Streptococcus pneumoniae is a manganese-dependent regulator, negatively affecting the expression of at least seven genes. Here, we extended these observations by transcriptome and proteome analysis of psaR mutants in strains D39 and TIGR4. The microarray analysis identified three shared PsaR targets: the psa-operon, pcpA, and prtA. Additionally, we found 31 genes to be regulated by PsaR in D39 only, most strikingly a cellobiose-specific PTS and a putative bacteriocin operon (sp0141-sp0146). In TIGR4, 14 PsaR gene targets were detected, with the rlrA pathogenicity islet being the most pronounced. Proteomics confirmed most of the shared gene targets. To examine the contribution of PsaR to pneumococcal virulence, we compared D39 and TIGR4 wild-type (wt) and psaR-mutants in three murine infection models. During colonization, no clear effect was observed of the psaR mutation in either D39 or TIGR4. In the pneumonia model, small but significant differences were observed in the lungs of mice infected with either D39wt or {triangleup}psaR: D39{triangleup}psaR had an initial advantage in survival in the lungs. Conversely, TIGR4{triangleup}psaR-infected mice had significantly lower bacterial loads at 24h only. Finally, during experimental bacteremia, D39{triangleup}psaR-infected mice had significantly lower bacterial loads in the blood stream than wt-infected mice for the first 24h of infection. TIGR4{triangleup}psaR showed attenuation at 36h only. In conclusion, our results show that PsaR of D39 and TIGR4 has a strain-specific role in global gene expression and in the development of bacteremia in mice.

4 E-mail: p.hermans{at}cukz.umcn.nl






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