ArticleCell host & microbe2020
Genome-Wide CRISPR Screen Identifies Semaphorin 6A and 6B as Receptors for Paeniclostridium sordellii Toxin TcsL.
Article in Cell host & microbe, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- Pathogenic mechanisms and resistance profiles of microbial pulmonary infections in lung cancer: a systematic review.BMC infectious diseases · 2025Pooled it
- Dissecting conserved molecular mechanisms of biological toxin activity through CRISPR screening.Biochemical Society transactions · 2026Review
- SEMA6A inhibits tumor progression and boosts anti-tumor immunity via blocking the ISG15/TGFβ axis in colorectal cancer.Molecular biomedicine · 2026Article
- High-throughput discovery of transmembrane helix dimers from human single-pass membrane proteins with TOXGREEN sort-seq.PNAS nexus · 2025Article
- De novo design of potent inhibitors of clostridial family toxins.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Design, performance, processing, and validation of a pooled CRISPR perturbation screen for bacterial toxins.Nature protocols · 2025Review
- The N-terminus of themBio · 2025Article
- The Cellular and Transcriptomic Early Innate Immune Response to BCG Vaccination in Mice.Cells · 2024Article
- Bacterial toxins induce non-canonical migracytosis to aggravate acute inflammation.Cell discovery · 2024Article
- Identification of a hemorrhagic determinant inMicrobiology spectrum · 2024Article
- Overview of Bacterial Protein Toxins from Pathogenic Bacteria: Mode of Action and Insights into Evolution.Toxins · 2024Review
- Molecular basis of TMPRSS2 recognition by Paeniclostridium sordellii hemorrhagic toxin.Nature communications · 2024Article
- Linking active rectal mucosa-attached microbiota to host immunity reveals its role in host-pathogenic STEC O157 interactions.The ISME journal · 2024Article
- An Updated View on the Cellular Uptake and Mode-of-Action of Clostridioides difficile Toxins.Advances in experimental medicine and biology · 2024Article
- Structural dynamics of the CROPs domain control stability and toxicity of Paeniclostridium sordellii lethal toxin.Nature communications · 2023Article
- Gaining New Insights into Fundamental Biological Pathways by Bacterial Toxin-Based Genetic Screens.Bioengineering (Basel, Switzerland) · 2023Review
- Receptor binding mechanisms of Clostridioides difficile toxin B and implications for therapeutics development.The FEBS journal · 2023Review
- Identification of TFPI as a receptor reveals recombination-driven receptor switching in Clostridioides difficile toxin B variants.Nature communications · 2022Article
- Alu Deletions inInternational journal of molecular sciences · 2022Article
- Paeniclostridium sordellii uterine infection is dependent on the estrous cycle.PLoS pathogens · 2022Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
The exotoxin TcsL is a major virulence factor in Paeniclostridium (Clostridium) sordellii and responsible for the high lethality rate associated with P. sordellii infection. Here, we present a genome-wide CRISPR-Cas9-mediated screen using a human lung carcinoma cell line and identify semaphorin (SEMA) 6A and 6B as receptors for TcsL. Disrupting SEMA6A/6B expression in several distinct human cell lines and primary human endothelial cells results in reduced TcsL sensitivity, while SEMA6A/6B over-expression increases their sensitivity. TcsL recognizes the extracellular domain (ECD) of SEMA6A/6B via a region homologous to the receptor-binding site in Clostridioides difficile toxin B (TcdB), which binds the human receptor Frizzled. Exchanging the receptor-binding interfaces between TcsL and TcdB switches their receptor-binding specificity. Finally, administration of SEMA6A-ECD proteins protects human cells from TcsL toxicity and reduces TcsL-induced damage to lung tissues and the lethality rate in mice. These findings establish SEMA6A and 6B as pathophysiologically relevant receptors for TcsL.
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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.