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Characterization and analysis of the Burkholderia pseudomallei BsaN virulence regulon

Yahua Chen, Imke Schröder, Christopher T French

  • 1Department of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117597, Singapore. yunn_hwen_gan@nuhs.edu.sg.

BMC Microbiology
|August 3, 2014
PubMed
Abstract

Insights

BsaN is a key regulator in Burkholderia pseudomallei, controlling virulence genes essential for pathogen survival within host cells. This study identifies its extensive regulon, revealing new targets and mechanisms for melioidosis pathogenesis.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Pathogen Biology

Background:

  • Burkholderia pseudomallei causes melioidosis, a significant human disease.
  • Type III (T3SS3) and Type VI (T6SS1) secretion systems are crucial for B. pseudomallei virulence.
  • BspR and BsaN are key regulators of these secretion systems.

Purpose of the Study:

  • To comprehensively define the regulatory targets of BsaN in B. pseudomallei.
  • To understand the role of BsaN in controlling virulence gene expression.
  • To elucidate the BsaN/BicA regulatory network.

Main Methods:

  • RNA sequencing (RNAseq) to compare wild-type and bsaN mutant transcriptomes.
  • Promoter-lacZ fusion assays in E. coli to study gene expression.
  • Mutagenesis to identify essential regulatory motifs.

Main Results:

  • BsaN positively regulates 60 genes, including polyketide and amino acid biosynthesis loci.
  • BsaN represses 51 genes, including flagellar motility and T3SS3 components.
  • BsaN and BicA directly regulate T3SS3 translocon, effector, and regulatory genes organized in at least five operons.
  • A consensus motif in promoter regions is essential for BsaN-mediated transcriptional activation.

Conclusions:

  • BsaN/BicA acts as a central regulator of critical virulence gene clusters in B. pseudomallei.
  • This regulatory network facilitates pathogen adaptation and intracellular survival.
  • BsaN/BicA controls a gene expression program vital for B. pseudomallei pathogenesis.

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