ArticleProceedings of the National Academy of Sciences of the United States of America2015
The adherens junctions control susceptibility to Staphylococcus aureus α-toxin.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 74 citations in OpenAlex.
- Acidic and alkaline conditions enhance Staphylococcus aureus α-toxin pore formation and cytotoxicity.PLoS pathogens · 2026Article
- Geometrically Constrained Growth Factor Concentration Favors Enrichment of Goblet Cells and Mucus Formation.ACS biomaterials science & engineering · 2026Article
- The Pathogenicity Mechanisms ofInternational journal of molecular sciences · 2025Review
- Strategies for Survival ofInternational journal of molecular sciences · 2025Review
- Combating multidrug-resistant (MDR) Staphylococcus aureus infection using terpene and its derivative.World journal of microbiology & biotechnology · 2024Review
- NArchives of microbiology · 2024Article
- Article
- The epithelial adherens junction component PLEKHA7 regulates ECM remodeling and cell behavior through miRNA-mediated regulation of MMP1 and LOX.bioRxiv : the preprint server for biology · 2024Article
- Changes functional prediction of ear canal flora in chronic bacterial otitis externa.Frontiers in cellular and infection microbiology · 2024Article
- The Staphylococcus aureus CamS lipoprotein is a repressor of toxin production that shapes host-pathogen interaction.PLoS biology · 2024Article
- Molecular Characteristics and Pathogenicity ofInternational journal of molecular sciences · 2023Review
- Inhibition of α-hemolysin activity of Staphylococcus aureus by theaflavin 3,3'-digallate.PloS one · 2023Article
- Airway Epithelial Cell Junctions as Targets for Pathogens and Antimicrobial Therapy.Pharmaceutics · 2022Review
- The ACE2 Receptor for Coronavirus Entry Is Localized at Apical Cell-Cell Junctions of Epithelial Cells.Cells · 2022Article
- Prevalence and Characterization of PVL-PositiveToxins · 2022Article
- Origin and Evolution of the Multifaceted Adherens Junction Component Plekha7.Frontiers in cell and developmental biology · 2022Article
- Phenotypic and Molecular Characterization of Bovine Mastitis Milk Origin Bacteria and Linkage of Intramammary Infection With Milk Quality.Frontiers in veterinary science · 2022Article
- PLEKHA7 signaling is necessary for the growth of mutant KRAS driven colorectal cancer.Experimental cell research · 2021Article
- Pathogenicity and virulence ofVirulence · 2021Review
- PLEKHA5, PLEKHA6, and PLEKHA7 bind to PDZD11 to target the Menkes ATPase ATP7A to the cell periphery and regulate copper homeostasis.Molecular biology of the cell · 2021Article
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17 authors at 3 institutions in 3 countries.
Funding
Abstract
Staphylococcus aureus is both a transient skin colonizer and a formidable human pathogen, ranking among the leading causes of skin and soft tissue infections as well as severe pneumonia. The secreted bacterial α-toxin is essential for S. aureus virulence in these epithelial diseases. To discover host cellular factors required for α-toxin cytotoxicity, we conducted a genetic screen using mutagenized haploid human cells. Our screen identified a cytoplasmic member of the adherens junctions, plekstrin-homology domain containing protein 7 (PLEKHA7), as the second most significantly enriched gene after the known α-toxin receptor, a disintegrin and metalloprotease 10 (ADAM10). Here we report a new, unexpected role for PLEKHA7 and several components of cellular adherens junctions in controlling susceptibility to S. aureus α-toxin. We find that despite being injured by α-toxin pore formation, PLEKHA7 knockout cells recover after intoxication. By infecting PLEKHA7(-/-) mice with methicillin-resistant S. aureus USA300 LAC strain, we demonstrate that this junctional protein controls disease severity in both skin infection and lethal S. aureus pneumonia. Our results suggest that adherens junctions actively control cellular responses to a potent pore-forming bacterial toxin and identify PLEKHA7 as a potential nonessential host target to reduce S. aureus virulence during epithelial infections.
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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.