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<p><i>Pseudomonas aeruginosa</i> is a ubiquitous, Gram-negative bacterium that forms biofilms and is responsible for antibiotic-resistant hospital-acquired infections in humans. The <i>P. aeruginosa</i> BqsRS two-component system regulates biofilm formation and dispersal by sensing extracytoplasmic Fe<sup>2+</sup>, but the mechanistic details of this process are poorly understood. In this work, we report the crystal and solution structures of the <i>Pa</i>BqsR response regulator receiver domain, comprising a (βα)<sub>5</sub> response regulator assembly, and the DNA-binding domain, comprising a helix-turn-helix motif. Consistent with its cognate stimulus being Fe<sup>2+</sup>, we show that <i>Pa</i>BqsR binds directly to the promoter region of the <i>feo</i> operon that encodes the bacterial Fe<sup>2+</sup> transport system FeoABC. Corroborating these in vitro results, transcriptional studies show that <i>Pa</i>BqsR is a global regulator controlling many important genes in PAO1, including the <i>feo</i> operon. Intriguingly, promoter-based assays reveal that <i>Pa</i>BqsR is a dynamic regulator that responds to bioavailable Fe<sup>2+</sup>, likely through the ability of <i>Pa</i>BqsR to bind Fe<sup>2+</sup> directly via a His-rich motif, independent of the <i>Pa</i>BqsS membrane His kinase. To our knowledge, this mode of regulation has not been reported previously among OmpR-like response regulators but represents an important level of control over Fe<sup>2+</sup> acquisition in <i>P. aeruginosa</i> that could be an attractive therapeutic target to treat hospital-acquired infections.</p>

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The response regulator BqsR/CarR controls Fe2+ acquisition in Pseudomonas aeruginosa

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月29日

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  • Alexander Paredes,
  • Mackenzie Hull,
  • Harvinder Singh,
  • Darryn Greene,
  • Ahmed O. Tajudeen,
  • Aya Kubo,
  • Sara Patamawenu,
  • Rachel Kramer,
  • Janae B. Brown,
  • Kelly N. Chacón,
  • Marianna A. Patrauchan,
  • Aaron T. Smith

摘要

Pseudomonas aeruginosa is a ubiquitous, Gram-negative bacterium that forms biofilms and is responsible for antibiotic-resistant hospital-acquired infections in humans. The P. aeruginosa BqsRS two-component system regulates biofilm formation and dispersal by sensing extracytoplasmic Fe2+, but the mechanistic details of this process are poorly understood. In this work, we report the crystal and solution structures of the PaBqsR response regulator receiver domain, comprising a (βα)5 response regulator assembly, and the DNA-binding domain, comprising a helix-turn-helix motif. Consistent with its cognate stimulus being Fe2+, we show that PaBqsR binds directly to the promoter region of the feo operon that encodes the bacterial Fe2+ transport system FeoABC. Corroborating these in vitro results, transcriptional studies show that PaBqsR is a global regulator controlling many important genes in PAO1, including the feo operon. Intriguingly, promoter-based assays reveal that PaBqsR is a dynamic regulator that responds to bioavailable Fe2+, likely through the ability of PaBqsR to bind Fe2+ directly via a His-rich motif, independent of the PaBqsS membrane His kinase. To our knowledge, this mode of regulation has not been reported previously among OmpR-like response regulators but represents an important level of control over Fe2+ acquisition in P. aeruginosa that could be an attractive therapeutic target to treat hospital-acquired infections.