ArticleCell2018
Programmed Secretion Arrest and Receptor-Triggered Toxin Export during Antibacterial Contact-Dependent Growth Inhibition.
Article in Cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 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.
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Who cites it
65 citing papers in PubMed, 87 citations in OpenAlex.
- In vitro reconstitution implicates multiple OMP assembly factors in CdiAThe Journal of biological chemistry · 2026Article
- Pathogenic Bordetella Bacteria Exploit Axonemal Microtubules to Penetrate the Ciliary Barrier.Cytoskeleton (Hoboken, N.J.) · 2026Article
- Bacterial weaponry and the ecological factors of competitive success.Essays in biochemistry · 2026Review
- Implications of proteome allocation constraints for understanding interbacterial antagonism.Microbiology (Reading, England) · 2026Review
- DeepPath: overcoming data scarcity for protein transition pathway prediction using physics-based deep learning.Chemical science · 2026Article
- Novel pESI-encoded autotransporter adhesin PeaP of epidemicbioRxiv : the preprint server for biology · 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
- Bacteria deliver a microtubule-binding protein into mammalian cells to promote colonization.Science (New York, N.Y.) · 2026Article
- First inhibitor of a bacterial two-partner secretion system.bioRxiv : the preprint server for biology · 2026Article
- An electron transport complex required in the gut sensitizesProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Proteolytically activated antibacterial toxins inhibit the growth of diverse gram-positive bacteria.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Surface protein machineries in Gram-negative bacteria.Journal of cell science · 2025Review
- An ex vivo Approach in European Seabass Leucocytes Supports the in vitro Regulation by Postbiotics of Aip56 Gene Expression of Photobacterium damselae subsp. piscicida.Probiotics and antimicrobial proteins · 2025Article
- Mechanism of activation of contact-dependent growth inhibition tRNase toxin by the amino acid biogenesis factor CysK in the bacterial competition system.Nucleic acids research · 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
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- Biocontrol of Escherichia coli O157:H7 by Enterobacter asburiae AEB30 on intact cantaloupe melons.Microbial biotechnology · 2024Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Contact-dependent growth inhibition (CDI) entails receptor-mediated delivery of CdiA-derived toxins into Gram-negative target bacteria. Using electron cryotomography, we show that each CdiA effector protein forms a filament extending ∼33 nm from the cell surface. Remarkably, the extracellular filament represents only the N-terminal half of the effector. A programmed secretion arrest sequesters the C-terminal half of CdiA, including the toxin domain, in the periplasm prior to target-cell recognition. Upon binding receptor, CdiA secretion resumes, and the periplasmic FHA-2 domain is transferred to the target-cell outer membrane. The C-terminal toxin region of CdiA then penetrates into the target-cell periplasm, where it is cleaved for subsequent translocation into the cytoplasm. Our findings suggest that the FHA-2 domain assembles into a transmembrane conduit for toxin transport into the periplasm of target bacteria. We propose that receptor-triggered secretion ensures that FHA-2 export is closely coordinated with integration into the target-cell outer membrane. VIDEO ABSTRACT.
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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.