ArticlePLoS biology2020
Pseudomonas aeruginosa cleaves the decoding center of Caenorhabditis elegans ribosomes.
Article in PLoS biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 18 citations in OpenAlex.
- Worming out defence strategies: mechanisms of immunity through the lens of genetic screens in C. elegans.Heredity · 2026Review
- Interplay between proteostasis pathways and innate immune responses inInfection and immunity · 2026Review
- The Pseudomonas aeruginosa ribonuclease Ribocin cleaves eukaryotic ribosomes at helix 69 to inhibit host translation.PLoS biology · 2026Article
- Identification of Pathogens and Biological Control of Wheat Fusarium Crown Rot in Xinjiang withMicroorganisms · 2026Article
- Intersections between proteostasis and immunity: insights from Caenorhabditis elegans.Disease models & mechanisms · 2026Review
- Patterns of pathogenesis in innate immunity: insights from C. elegans.Nature reviews. Immunology · 2025Review
- Cystatin antibodies interfere with ovary development in Haemaphysalis doenitzi (Acari: Ixodidae).PLoS neglected tropical diseases · 2025Article
- Eukaryotic Elongation Factor 2 Kinase EFK-1/eEF2K promotes starvation resistance by preventing oxidative damage in C. elegans.Nature communications · 2025Article
- Unzipping the defense: a comprehensive review on bZIP transcription factors inFrontiers in cellular and infection microbiology · 2025Review
- Material-based treatment strategies against intraosseous implant biofilm infection.Biochemistry and biophysics reports · 2024Review
- Modeling Host-Pathogen Interactions inInternational journal of molecular sciences · 2024Review
- An organismal understanding of C. elegans innate immune responses, from pathogen recognition to multigenerational resistance.Seminars in cell & developmental biology · 2024Review
- Nervous system guides behavioral immunity inPeerJ · 2024Review
- Oh my gut! Is the microbial origin of neurodegenerative diseases real?Infection and immunity · 2023Review
- C. elegans: out on an evolutionary limb.Immunogenetics · 2022Review
- Pseudomonas aeruginosa PA14 produces R-bodies, extendable protein polymers with roles in host colonization and virulence.Nature communications · 2021Article
Corrections and comments
- Updated by
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Pathogens such as Pseudomonas aeruginosa advantageously modify animal host physiology, for example, by inhibiting host protein synthesis. Translational inhibition of insects and mammalian hosts by P. aeruginosa utilizes the well-known exotoxin A effector. However, for the infection of Caenorhabditis elegans by P. aeruginosa, the precise pathways and mechanism(s) of translational inhibition are not well understood. We found that upon exposure to P. aeruginosa PA14, C. elegans undergoes a rapid loss of intact ribosomes accompanied by the accumulation of ribosomes cleaved at helix 69 (H69) of the 26S ribosomal RNA (rRNA), a key part of ribosome decoding center. H69 cleavage is elicited by certain virulent P. aeruginosa isolates in a quorum sensing (QS)-dependent manner and independently of exotoxin A-mediated translational repression. H69 cleavage is antagonized by the 3 major host defense pathways defined by the pmk-1, fshr-1, and zip-2 genes. The level of H69 cleavage increases with the bacterial exposure time, and it is predominantly localized in the worm's intestinal tissue. Genetic and genomic analysis suggests that H69 cleavage leads to the activation of the worm's zip-2-mediated defense response pathway, consistent with translational inhibition. Taken together, our observations suggest that P. aeruginosa deploys a virulence mechanism to induce ribosome degradation and H69 cleavage of host ribosomes. In this manner, P. aeruginosa would impair host translation and block antibacterial responses.
Indexed as
Identifiers
What Socratic 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 Socratic graph.