ArticlePLoS biology2016
Structural and Molecular Mechanism of CdpR Involved in Quorum-Sensing and Bacterial Virulence in Pseudomonas aeruginosa.
Article in PLoS biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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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.
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Who cites it
38 citing papers in PubMed, 59 citations in OpenAlex.
- Regulatory cascade of NdpR and NdpR2 in controlling nicotine degradation operons inApplied and environmental microbiology · 2026Article
- Characterization of hypothetical proteins reveals function modules and virulence factors in Pseudomonas aeruginosa.Nature communications · 2026Article
- A genome-wide screen inJournal of bacteriology · 2026Article
- Simultaneous inhibition of bacterial virulence and anti-phage defense systems by synergistic bacteriophage counter-defense proteins.The EMBO journal · 2026Article
- Transcriptional profiling ofFrontiers in microbiology · 2026Article
- A plasmid-encoded inactive toxin-antitoxin system MtvT/MtvA regulates plasmid conjugative transfer and bacterial virulence in Pseudomonas aeruginosa.Nucleic acids research · 2025Article
- Understanding the pathophysiology ofBurns & trauma · 2025Review
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- Z3495, a LysR-Type Transcriptional Regulator Encoded in O Island 97, Regulates Virulence Gene Expression in EnterohemorrhagicMicroorganisms · 2024Article
- The transcriptional regulators of virulence forGenes & diseases · 2023Review
- Transcriptional Regulators Controlling Virulence inInternational journal of molecular sciences · 2023Review
- Mechanisms regulating the CRISPR-Cas systems.Frontiers in microbiology · 2023Review
- PmiR senses 2-methylisocitrate levels to regulate bacterial virulence inScience advances · 2022Article
- Pf4 Phage Variant Infection Reduces Virulence-Associated Traits inMicrobiology spectrum · 2022Article
- Pseudomonas aeruginosa: pathogenesis, virulence factors, antibiotic resistance, interaction with host, technology advances and emerging therapeutics.Signal transduction and targeted therapy · 2022Review
- Proteomic profiling spotlights the molecular targets and the impact of the natural antivirulent umbelliferone on stress response, virulence factors, and the quorum sensing network ofFrontiers in cellular and infection microbiology · 2022Article
- AraC-type regulators HilC and RtsA are directly controlled by an intestinal fatty acid to regulate Salmonella invasion.Molecular microbiology · 2021Article
- ClpP1P2 peptidase activity promotes biofilm formation in Pseudomonas aeruginosa.Molecular microbiology · 2021Article
- The AraC-Type Transcriptional Regulator GliR (PA3027) Activates Genes of Glycerolipid Metabolism inInternational journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
9 authors at 6 institutions in 2 countries.
Funding
Abstract
Although quorum-sensing (QS) systems are important regulators of virulence gene expression in the opportunistic human pathogen Pseudomonas aeruginosa, their detailed regulatory mechanisms have not been fully characterized. Here, we show that deletion of PA2588 resulted in increased production of pyocyanin and biofilm, as well as enhanced pathogenicity in a mouse model. To gain insights into the function of PA2588, we performed a ChIP-seq assay and identified 28 targets of PA2588, including the intergenic region between PA2588 and pqsH, which encodes the key synthase of Pseudomonas quinolone signal (PQS). Though the C-terminal domain was similar to DNA-binding regions of other AraC family members, structural studies revealed that PA2588 has a novel fold at the N-terminal region (NTR), and its C-terminal HTH (helix-turn-helix) domain is also unique in DNA recognition. We also demonstrated that the adaptor protein ClpS, an essential regulator of ATP-dependent protease ClpAP, directly interacted with PA2588 before delivering CdpR to ClpAP for degradation. We named PA2588 as CdpR (ClpAP-degradation and pathogenicity Regulator). Moreover, deletion of clpP or clpS/clpA promotes bacterial survival in a mouse model of acute pneumonia infection. Taken together, this study uncovered that CdpR is an important QS regulator, which can interact with the ClpAS-P system to regulate the expression of virulence factors and pathogenicity.
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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.