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<p>Chemoreceptors enable bacteria to modulate their swimming behavior in response to the perceived environmental cues. Despite the large diversity of stimuli sensed by bacterial chemoreceptors, their output to the chemotaxis pathway that controls the flagellar motor typically converges on a few conserved signaling proteins. Here, we characterize a unique chemoreceptor-like protein, Tls, which is found in the B2 phylogroup of <i>Escherichia coli</i> that includes many extraintestinal pathogenic (ExPEC) strains. Instead of mediating chemotactic signaling, Tls controls motility by repressing the expression of flagellar genes, and thus cell motility, through sequestration of the transcriptional master activator of flagellar genes, FlhDC. The subcellular localization of Tls, the sequestration of FlhDC, and the repression of flagellar gene expression and motility are all abolished during growth on porous medium, indicating that this regulation may be mechanosensitive. Deletion of <i>tls</i> in a uropathogenic <i>E. coli</i> strain leads to reduced attachment to the urinary tract cells and an increased migration to and/or proliferation in the murine gut, a pathogen reservoir niche, thus implicating Tls in the regulation of motility during infection.</p>

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Control of flagellar gene expression by a chemotaxis receptor-like regulator in pathogenic Escherichia coli

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年10月13日

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  • Jae-Woo Lee,
  • Liyun Wang,
  • Sarah L Comer,
  • Remy Colin,
  • Mollie M Gidney,
  • Leanid Laganenka,
  • Wolf-Dietrich Hardt,
  • Maria Hadjifrangiskou,
  • Victor Sourjik

摘要

Chemoreceptors enable bacteria to modulate their swimming behavior in response to the perceived environmental cues. Despite the large diversity of stimuli sensed by bacterial chemoreceptors, their output to the chemotaxis pathway that controls the flagellar motor typically converges on a few conserved signaling proteins. Here, we characterize a unique chemoreceptor-like protein, Tls, which is found in the B2 phylogroup of Escherichia coli that includes many extraintestinal pathogenic (ExPEC) strains. Instead of mediating chemotactic signaling, Tls controls motility by repressing the expression of flagellar genes, and thus cell motility, through sequestration of the transcriptional master activator of flagellar genes, FlhDC. The subcellular localization of Tls, the sequestration of FlhDC, and the repression of flagellar gene expression and motility are all abolished during growth on porous medium, indicating that this regulation may be mechanosensitive. Deletion of tls in a uropathogenic E. coli strain leads to reduced attachment to the urinary tract cells and an increased migration to and/or proliferation in the murine gut, a pathogen reservoir niche, thus implicating Tls in the regulation of motility during infection.