ReviewCold Spring Harbor perspectives in medicine2014
Mechanisms and biological roles of contact-dependent growth inhibition systems.
Review in Cold Spring Harbor perspectives in medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
What it found
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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.
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
63 citing papers in PubMed, 100 citations in OpenAlex.
- Review
- Microbial GAIN domains undergo autoproteolysis and enable release of diverse cell-surface-associated proteins.Current biology : CB · 2026Article
- ABPs: diffusible antibacterial toxins secreted by and active against diverse gram-positive bacteria.Infection and immunity · 2026Review
- Contact dependent suppression ofbioRxiv : the preprint server for biology · 2026Article
- The yxiD gene from Bacillus subtilis 6633 encodes a polymorphic toxin with tRNase activity and is neutralized by the cognate immunity protein YxxD.Nucleic acids research · 2025Article
- Cross-kingdom dialogs in the gut: Integrating bacterial pathogens, helminths, and microbiota interactions for immune homeostasis.PLoS pathogens · 2025Review
- Working together: gut microbe-microbe interactions shape host inflammation.Infection and immunity · 2025Review
- The Competitive Edge: T6SS-Mediated Interference Competition byMicroorganisms · 2025Review
- Dietary amino acids regulate Salmonella colonization via microbiota-dependent mechanisms in the mouse gut.Nature communications · 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
- The dominant lineage of an emerging pathogen harbours contact-dependent inhibition systems.Microbial genomics · 2025Article
- Harnessing the human gut microbiota: an emerging frontier in combatting multidrug-resistant bacteria.Frontiers in immunology · 2025Review
- Conservation and similarity of bacterial and eukaryotic innate immunity.Nature reviews. Microbiology · 2024Review
- Article
- The microbiota: a crucial mediator in gut homeostasis and colonization resistance.Frontiers in microbiology · 2024Review
- Structural and functional insights into the delivery of a bacterial Rhs pore-forming toxin to the membrane.Nature communications · 2023Article
- Microbiota-mediated colonization resistance: mechanisms and regulation.Nature reviews. Microbiology · 2023Review
- The type-VI secretion system of the beneficial symbiontMicrobiology (Reading, England) · 2023Review
- Antibacterial contact-dependent proteins secreted by Gram-negative cystic fibrosis respiratory pathogens.Trends in microbiology · 2022Review
- Mechanistic insights into tRNA cleavage by a contact-dependent growth inhibitor protein and translation factors.Nucleic acids research · 2022Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Bacterial contact-dependent growth inhibition (CDI) is mediated by the CdiA/CdiB family of two-partner secretion proteins. CDI(+) cells bind to susceptible target bacteria and deliver a toxic effector domain derived from the carboxyl terminus of CdiA (CdiA-CT). More than 60 distinct CdiA-CT sequence types have been identified, and all CDI toxins characterized thus far display RNase, DNase, or pore-forming activities. CDI systems also encode CdiI immunity proteins, which specifically bind and inactivate cognate CdiA-CT toxins to prevent autoinhibition. CDI activity appears to be limited to target cells of the same species, suggesting that these systems play a role in competition between closely related bacteria. Recent work on the CDI system from uropathogenic Escherichia coli (UPEC 536) has revealed that its CdiA-CT toxin binds tightly to a cysteine biosynthetic enzyme (CysK) in the cytoplasm of target cells. The unanticipated complexity in the UPEC CDI pathway raises the possibility that these systems perform other functions in addition to growth inhibition. Finally, we propose that the phenomenon of CDI is more widespread than previously appreciated. Rhs (rearrangement hotspot) systems encode toxin-immunity pairs, some of which share significant sequence identity with CdiA-CT/CdiI proteins. A number of recent observations suggest that Rhs proteins mediate a distinct form of CDI.
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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.