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Background <p>The <i>Caenorhabditis elegans–Escherichia coli</i> system is advantageous for studying host-microbe interactions at the single-gene level. By screening with this system, we identified that the deletion of <i>cpxR</i>, an <i>E. coli</i> transcription factor for the envelope stress response, delays <i>C. elegans</i> development. This finding led us to investigate how this gene regulates host development.</p> Results <p>We identified that <i>E. coli</i> Δ<i>cpxR</i> induced <i>C. elegans</i> developmental delay and activated the <i>C. elegans</i> mitochondrial unfolded protein response pathway through reactive oxygen species. It is widely accepted that the Cpx system is important for bacterial pathogenesis, and activating CpxR is regarded as an antimicrobial strategy. Moreover, we discovered that Δ<i>cpxR</i> cultured in LB medium, not cultured in M9 minimal medium, delayed <i>C. elegans</i> development, and the L-histidine-related metabolism of Δ<i>cpxR</i> contributed mostly to the difference. The metabolic fluctuations of commensal bacteria reveal that, rather than the activation of the <i>E. coli</i> Cpx response, the dynamic response of the <i>E. coli</i> Cpx system really contributes to <i>C. elegans</i> development. Furthermore, as the concentration of <i>N</i>-acetylcysteine increased, the phenotype of <i>C. elegans</i> fed Δ<i>cpxR</i> transitioned from developmental delay to survival resistance. The dynamic response is also indicated in the process in which commensal <i>E. coli</i> improves the stress tolerance of the host <i>C. elegans</i> to <i>N</i>-acetylcysteine.</p> Conclusions <p>Our results illustrate that environmental factors can shape the regulation of the <i>E. coli</i> Cpx response to <i>C. elegans</i>, providing new evidence for why Cpx-mediated virulence phenotypes are inconsistent among gram-negative species in different ecological niches.</p>

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Dynamic response by commensal E. coli two-component system Cpx contributes to C. elegans development

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月3日

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  • Huiyang Xiong,
  • Beilei Hua,
  • Huanhu Zhu

摘要

Background

The Caenorhabditis elegans–Escherichia coli system is advantageous for studying host-microbe interactions at the single-gene level. By screening with this system, we identified that the deletion of cpxR, an E. coli transcription factor for the envelope stress response, delays C. elegans development. This finding led us to investigate how this gene regulates host development.

Results

We identified that E. coli ΔcpxR induced C. elegans developmental delay and activated the C. elegans mitochondrial unfolded protein response pathway through reactive oxygen species. It is widely accepted that the Cpx system is important for bacterial pathogenesis, and activating CpxR is regarded as an antimicrobial strategy. Moreover, we discovered that ΔcpxR cultured in LB medium, not cultured in M9 minimal medium, delayed C. elegans development, and the L-histidine-related metabolism of ΔcpxR contributed mostly to the difference. The metabolic fluctuations of commensal bacteria reveal that, rather than the activation of the E. coli Cpx response, the dynamic response of the E. coli Cpx system really contributes to C. elegans development. Furthermore, as the concentration of N-acetylcysteine increased, the phenotype of C. elegans fed ΔcpxR transitioned from developmental delay to survival resistance. The dynamic response is also indicated in the process in which commensal E. coli improves the stress tolerance of the host C. elegans to N-acetylcysteine.

Conclusions

Our results illustrate that environmental factors can shape the regulation of the E. coli Cpx response to C. elegans, providing new evidence for why Cpx-mediated virulence phenotypes are inconsistent among gram-negative species in different ecological niches.