ArticleJournal of bacteriology2013
The Cpx stress response confers resistance to some, but not all, bactericidal antibiotics.
Article in Journal of bacteriology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
60 citing papers in PubMed, 107 citations in OpenAlex.
- Phenotypic Effects of a Small Molecule CpxA Phosphatase Inhibitor on Uropathogenic Escherichia coli.ACS infectious diseases · 2026Article
- Reactive oxygen detoxification contributes toeLife · 2026Article
- Robust antibiotic sensitization of pathogenic Pseudomonas aeruginosa via negative hysteresis in the cell envelope.Nature communications · 2026Article
- A widely-occurring family of pore-forming effectors broadens the impact of the Serratia Type VI secretion system.The EMBO journal · 2025Article
- A dual-mechanism antimicrobial peptide with antimutagenic activity targets the replisome and induces cell envelope stress.mSphere · 2025Article
- Gut Microbiota and Neurodevelopment in Preterm Infants: Mechanistic Insights and Prospects for Clinical Translation.Microorganisms · 2025Review
- CRISPRi screening revealsmSystems · 2025Article
- Antibiotic-induced stress responses in Gram-negative bacteria and their role in antibiotic resistance.The Journal of antimicrobial chemotherapy · 2025Review
- Aminoglycoside heteroresistance inmBio · 2024Article
- Regulatory role of the Cpx ESR in bacterial behaviours.Virulence · 2024Review
- Cpx-signalling innpj antimicrobials and resistance · 2024Article
- RavA-ViaA antibiotic response is linked to Cpx and Zra2 envelope stress systems inMicrobiology spectrum · 2023Article
- Are envelope stress responses essential for persistence to β-lactams inAntimicrobial agents and chemotherapy · 2023Article
- Nutrient Limitation SensitizesACS infectious diseases · 2023Article
- In Vivo Role of Two-Component Regulatory Systems in Models of Urinary Tract Infections.Pathogens (Basel, Switzerland) · 2023Review
- YihE is a novel binding partner of Rho and regulates Rho-dependent transcription termination in the Cpx stress response.iScience · 2022Article
- Targeting the Holy Triangle of Quorum Sensing, Biofilm Formation, and Antibiotic Resistance in Pathogenic Bacteria.Microorganisms · 2022Review
- Gram-Negative Bacterial Envelope Homeostasis under Oxidative and Nitrosative Stress.Microorganisms · 2022Review
- Collateral Sensitivity Interactions between Antibiotics Depend on Local Abiotic Conditions.mSystems · 2021Article
- Role ofFrontiers in microbiology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
It has recently been suggested that bactericidal antibiotics, including aminoglycoside antibiotics (AGAs), and toxic small molecules, such as hydroxyurea (HU), kill bacteria the same way, namely, by generating reactive oxygen species (ROS) via a process requiring activation of the Cpx stress response. We suggest an opposite, protective role for Cpx. We have confirmed the initial finding that cpxA null mutations confer resistance to HU. However, the two-component sensor CpxA is both a kinase and a phosphatase, and previous work from our lab has shown that removing CpxA can activate the stress response owing to buildup of the phosphorylated response regulator (CpxR∼P) that occurs in the absence of the phosphatase activity. We show that a dominant cpxA* mutation that constitutively activates the Cpx stress response confers a high level of resistance to both HU and AGAs in a CpxR-dependent manner. In contrast, inactivating the CpxR response regulator by mutating the phosphorylation site (D51A) or the putative DNA-binding motif (M199A) does not increase resistance to HU or AGAs. Taken together, these results demonstrate that activation of the Cpx stress response can protect cells from HU and AGAs. However, the Cpx response does not increase resistance to all classes of bactericidal antibiotics, as the cpxA* mutants are not significantly more resistant to fluoroquinolones or β-lactams than wild-type cells. Thus, it seems unlikely that all bactericidal antibiotics kill by the same mechanism.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.