ArticleProceedings of the National Academy of Sciences of the United States of America2014
Clostridium difficile toxin CDT hijacks microtubule organization and reroutes vesicle traffic to increase pathogen adherence.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 96 citations in OpenAlex.
- From colonization to infection: Genomic evolution of Clostridioides difficile pathogenesis.Cell reports · 2026Review
- Nanobodies against Clostridioides difficile CDTb provide a toolkit for potent toxin neutralization and highly sensitive quantitation.The Journal of biological chemistry · 2026Article
- Comparative genomic analysis of Clostridioides difficile strains in Mexico: insights into virulence and resistance.Access microbiology · 2026Article
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- Unravelling three-way interactions betweenJournal of medical microbiology · 2025Review
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- Article
- The phi027 bacteriophage influences physiology and virulence of the lysogenic strain of Clostridioides difficile.Scientific reports · 2025Article
- The evolving landscape of live biotherapeutics in the treatment of Clostridioides difficile infection.Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology · 2025Review
- Article
- Decoding the role of microtubules: a trafficking road for vesicle.Theranostics · 2025Review
- An Updated View on the Cellular Uptake and Mode-of-Action of Clostridioides difficile Toxins.Advances in experimental medicine and biology · 2024Article
- Immunization Strategies Against Clostridioides difficile.Advances in experimental medicine and biology · 2024Review
- Pathogenicity and virulence ofVirulence · 2023Review
- Discrimination between hypervirulent and non-hypervirulent ribotypes of Clostridioides difficile by MALDI-TOF mass spectrometry and machine learning.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2023Article
- Review
- Redistribution of the Novel Clostridioides difficile Spore Adherence Receptor E-Cadherin by TcdA and TcdB Increases Spore Binding to Adherens Junctions.Infection and immunity · 2023Article
- Article
- Identification of TFPI as a receptor reveals recombination-driven receptor switching in Clostridioides difficile toxin B variants.Nature communications · 2022Article
- Cryo-EM structures of the translocational binary toxin complex CDTa-bound CDTb-pore from Clostridioides difficile.Nature communications · 2022Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Clostridium difficile causes antibiotic-associated diarrhea and pseudomembranous colitis by the actions of Rho-glucosylating toxins A and B. Recently identified hypervirulent strains, which are associated with increased morbidity and mortality, additionally produce the actin-ADP-ribosylating toxin C. difficile transferase (CDT). CDT depolymerizes actin, causes formation of microtubule-based protrusions, and increases pathogen adherence. Here we show that CDT-induced protrusions allow vesicle traffic and contain endoplasmic reticulum tubules, connected to microtubules via the calcium sensor Stim1. The toxin reroutes Rab11-positive vesicles containing fibronectin, which is involved in bacterial adherence, from basolateral to the apical membrane sides in a microtubule- and Stim1-dependent manner. The data yield a model of C. difficile adherence regulated by actin depolymerization, microtubule restructuring, subsequent Stim1-dependent Ca(2+) signaling, vesicle rerouting, and secretion of ECM proteins to increase bacterial adherence.
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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.