ArticlePLoS pathogens2016
CdiA Effectors from Uropathogenic Escherichia coli Use Heterotrimeric Osmoporins as Receptors to Recognize Target Bacteria.
Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed, 51 citations in OpenAlex.
- Phylogenomic framework and virulence gene boundaries of emerging Shiga toxin-producingVirulence · 2026Article
- In vitro reconstitution implicates multiple OMP assembly factors in CdiAThe Journal of biological chemistry · 2026Article
- C-terminal domain of the filamentous hemagglutinin FhaB is crucial for interaction ofbioRxiv : the preprint server for biology · 2026Article
- Elongation Factor Tu Acts as a Chaperone to Activate an Antibacterial RNase Toxin.Molecular microbiology · 2026Article
- Surface protein machineries in Gram-negative bacteria.Journal of cell science · 2025Review
- The Competitive Edge: T6SS-Mediated Interference Competition byMicroorganisms · 2025Review
- PorV factor of the type IX secretion system and PosF porin act as adhesins in Riemerella anatipestifer infection.Veterinary research · 2025Article
- The dominant lineage of an emerging pathogen harbours contact-dependent inhibition systems.Microbial genomics · 2025Article
- Contact-dependent growth inhibition (CDI) systems deploy a large family of polymorphic ionophoric toxins for inter-bacterial competition.PLoS genetics · 2024Article
- Autoproteolytic mechanism of CdiA toxin release reconstitutedJournal of bacteriology · 2024Article
- Glyoxylate Shunt and Pyruvate-to-Acetoin Shift Are Specific Stress Responses Induced by Colistin and Ceragenin CSA-13 in Enterobacter hormaechei ST89.Microbiology spectrum · 2023Article
- The Role of Outer Membrane Proteins in UPEC Antimicrobial Resistance: A Systematic Review.Membranes · 2022Review
- Antibacterial contact-dependent proteins secreted by Gram-negative cystic fibrosis respiratory pathogens.Trends in microbiology · 2022Review
- Recipient Cell Factors Influence Interbacterial Competition Mediated by Two Distinct Burkholderia dolosa Contact-Dependent Growth Inhibition Systems.Journal of bacteriology · 2022Article
- Probiotic Escherichia coli Nissle 1917 inhibits bacterial persisters that survive fluoroquinolone treatment.Journal of applied microbiology · 2022Article
- Functional and Structural Diversity of Bacterial Contact-Dependent Growth Inhibition Effectors.Frontiers in molecular biosciences · 2022Review
- Antimicrobial Weapons of Pseudomonas aeruginosa.Advances in experimental medicine and biology · 2022Article
- Article
- Article
- Contact-Dependent Growth Inhibition in Bacteria: Do Not Get Too Close!International journal of molecular sciences · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Many Gram-negative bacterial pathogens express contact-dependent growth inhibition (CDI) systems that promote cell-cell interaction. CDI+ bacteria express surface CdiA effector proteins, which transfer their C-terminal toxin domains into susceptible target cells upon binding to specific receptors. CDI+ cells also produce immunity proteins that neutralize the toxin domains delivered from neighboring siblings. Here, we show that CdiAEC536 from uropathogenic Escherichia coli 536 (EC536) uses OmpC and OmpF as receptors to recognize target bacteria. E. coli mutants lacking either ompF or ompC are resistant to CDIEC536-mediated growth inhibition, and both porins are required for target-cell adhesion to inhibitors that express CdiAEC536. Experiments with single-chain OmpF fusions indicate that the CdiAEC536 receptor is heterotrimeric OmpC-OmpF. Because the OmpC and OmpF porins are under selective pressure from bacteriophages and host immune systems, their surface-exposed loops vary between E. coli isolates. OmpC polymorphism has a significant impact on CDIEC536 mediated competition, with many E. coli isolates expressing alleles that are not recognized by CdiAEC536. Analyses of recombinant OmpC chimeras suggest that extracellular loops L4 and L5 are important recognition epitopes for CdiAEC536. Loops L4 and L5 also account for much of the sequence variability between E. coli OmpC proteins, raising the possibility that CDI contributes to the selective pressure driving OmpC diversification. We find that the most efficient CdiAEC536 receptors are encoded by isolates that carry the same cdi gene cluster as E. coli 536. Thus, it appears that CdiA effectors often bind preferentially to "self" receptors, thereby promoting interactions between sibling cells. As a consequence, these effector proteins cannot recognize nor suppress the growth of many potential competitors. These findings suggest that self-recognition and kin selection are important functions of CDI.
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.