ArticleCell reports2021
Thiol-based functional mimicry of phosphorylation of the two-component system response regulator ArcA promotes pathogenesis in enteric pathogens.
Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- EnterohemorrhagiciScience · 2026Article
- sRNA centered signaling activates nitrate respiration and enhances Cronobacter sakazakii virulence in host environments.Nature communications · 2026Article
- In Vivo Nitrosative Stress-Induced Expression of a Photolyase Promotes Vibrio cholerae Environmental Blue Light Resistance.Molecular microbiology · 2025Article
- The ArcB kinase sensor participates in the phagocyte-mediated stress response inFrontiers in microbiology · 2025Article
- A novel computational approach for the mining of signature pathways using species co-occurrence networks in gut microbiomes.BMC microbiology · 2024Article
- Trade-offs between receptor modification and fitness drive host-bacteriophage co-evolution leading to phage extinction or co-existence.The ISME journal · 2024Article
- Central metabolism is a key player in E. coli biofilm stimulation by sub-MIC antibiotics.PLoS genetics · 2023Article
- The use of RNA-based treatments in the field of cancer immunotherapy.Molecular cancer · 2023Review
- The ArcAB Two-Component System: Function in Metabolism, Redox Control, and Infection.Microbiology and molecular biology reviews : MMBR · 2022Review
- S-Nitrosylation of the virulence regulator AphB promotes Vibrio cholerae pathogenesis.PLoS pathogens · 2022Article
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Pathogenic bacteria can rapidly respond to stresses such as reactive oxygen species (ROS) using reversible redox-sensitive oxidation of cysteine thiol (-SH) groups in regulators. Here, we use proteomics to profile reversible ROS-induced thiol oxidation in Vibrio cholerae, the etiologic agent of cholera, and identify two modified cysteines in ArcA, a regulator of global carbon oxidation that is phosphorylated and activated under low oxygen. ROS abolishes ArcA phosphorylation but induces the formation of an intramolecular disulfide bond that promotes ArcA-ArcA interactions and sustains activity. ArcA cysteines are oxidized in cholera patient stools, and ArcA thiol oxidation drives in vitro ROS resistance, colonization of ROS-rich guts, and environmental survival. In other pathogens, such as Salmonella enterica, oxidation of conserved cysteines of ArcA orthologs also promotes ROS resistance, suggesting a common role for ROS-induced ArcA thiol oxidation in modulating ArcA activity, allowing for a balance of expression of stress- and pathogenesis-related genetic programs.
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