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Regulation of PI-2b Pilus Expression in Hypervirulent Streptococcus agalactiae ST-17 BM110

Bruno Périchon1,2, Noémi Szili1,2, Laurence du Merle1,2

  • 1Institut Pasteur, Biology of Gram-positive Pathogens Unit, Paris, France.

Plos One
|January 21, 2017
PubMed

Insights

A hairpin structure regulates PI-2b pilus expression in hypervirulent Streptococcus agalactiae (GBS) ST17 strains. Deleting this hairpin increases PI-2b transcription, potentially enhancing GBS virulence and dissemination in neonatal meningitis.

Area of Science:

  • Microbiology
  • Genetics
  • Molecular Biology

Background:

  • Streptococcus agalactiae (Group B Streptococcus, GBS) ST17 clone is linked to neonatal meningitis.
  • The PI-2b locus is common in ST17 strains and some non-ST17 isolates.

Purpose of the Study:

  • Analyze PI-2b pilus expression differences between ST17 (BM110) and non-ST17 (A909) GBS strains.
  • Investigate the role of a specific hairpin structure in regulating PI-2b expression.

Main Methods:

  • Comparative genome analysis to identify genetic differences.
  • RNA sequencing (RNAseq), primer extension, qRT-PCR, and GFP reporter gene assays.
  • Gene reporter assays in Lactococcus lactis.

Main Results:

  • A 43-bp hairpin structure upstream of PI-2b operon is present in ST17 strains but absent in non-ST17 strains.
  • Deletion of the hairpin in BM110 increased PI-2b transcription 3- to 5-fold.
  • The hairpin acts as a transcriptional terminator; read-through from the antigen B operon may influence PI-2b expression in A909.
  • GBS-specific regulatory factors are necessary for PI-2b transcription.

Conclusions:

  • PI-2b expression is tightly regulated in GBS ST17 strains, likely via the identified hairpin structure.
  • This regulation may provide a selective advantage to GBS ST17, potentially by modulating host immune responses or increasing dissemination.

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