ArticlePLoS pathogens2010
Bordetella adenylate cyclase toxin mobilizes its beta2 integrin receptor into lipid rafts to accomplish translocation across target cell membrane in two steps.
Article in PLoS pathogens, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 97 citations in OpenAlex.
- Acyl chains stabilize the acylated domain and determine the receptor-mediated interaction of the Bordetella adenylate cyclase toxin with cell membrane.The Journal of biological chemistry · 2025Article
- Environmental Toxicants and Their Disruption of Integrin Signaling in Lipid Rafts.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Eosinophils as drivers of bacterial immunomodulation and persistence.Infection and immunity · 2024Review
- cAMP signaling ofmSphere · 2024Article
- Some Examples of Bacterial Toxins as Tools.Toxins · 2024Review
- Membrane Interaction Characteristics of the RTX Toxins and the Cholesterol-Dependence of Their Cytolytic/Cytotoxic Activity.International journal of molecular sciences · 2024Review
- CyaA translocation across eukaryotic cell membranes.Frontiers in molecular biosciences · 2024Article
- Heterologously secreted MbxA from Moraxella bovis induces a membrane blebbing response of the human host cell.Scientific reports · 2022Article
- Four Cholesterol-Recognition Motifs in the Pore-Forming and Translocation Domains of Adenylate Cyclase Toxin Are Essential for Invasion of Eukaryotic Cells and Lysis of Erythrocytes.International journal of molecular sciences · 2022Article
- Templated folding of the RTX domain of the bacterial toxin adenylate cyclase revealed by single molecule force spectroscopy.Nature communications · 2022Article
- Review
- Cholesterol stimulates the lytic activity of Adenylate Cyclase Toxin on lipid membranes by promoting toxin oligomerization and formation of pores with a greater effective size.The FEBS journal · 2021Article
- Different roles of conserved tyrosine residues of the acylated domains in folding and activity of RTX toxins.Scientific reports · 2021Article
- Almost half of the RTX domain is dispensable for complement receptor 3 binding and cell-invasive activity of the Bordetella adenylate cyclase toxin.The Journal of biological chemistry · 2021Article
- A High-Affinity Calmodulin-Binding Site in the CyaA Toxin Translocation Domain is Essential for Invasion of Eukaryotic Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Article
- Molecular detection and phylogenetic analysis ofNew microbes and new infections · 2020Article
- Retargeting from the CR3 to the LFA-1 receptor uncovers the adenylyl cyclase enzyme-translocating segment ofThe Journal of biological chemistry · 2020Article
- Aggregatibacter actinomycetemcomitans leukotoxin: From mechanism to targeted anti-toxin therapeutics.Molecular oral microbiology · 2020Review
- Review
- Adenylate Cyclase Toxin Tinkering With Monocyte-Macrophage Differentiation.Frontiers in immunology · 2020Review
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bordetella adenylate cyclase toxin (CyaA) binds the alpha(M)beta(2) integrin (CD11b/CD18, Mac-1, or CR3) of myeloid phagocytes and delivers into their cytosol an adenylate cyclase (AC) enzyme that converts ATP into the key signaling molecule cAMP. We show that penetration of the AC domain across cell membrane proceeds in two steps. It starts by membrane insertion of a toxin 'translocation intermediate', which can be 'locked' in the membrane by the 3D1 antibody blocking AC domain translocation. Insertion of the 'intermediate' permeabilizes cells for influx of extracellular calcium ions and thus activates calpain-mediated cleavage of the talin tether. Recruitment of the integrin-CyaA complex into lipid rafts follows and the cholesterol-rich lipid environment promotes translocation of the AC domain across cell membrane. AC translocation into cells was inhibited upon raft disruption by cholesterol depletion, or when CyaA mobilization into rafts was blocked by inhibition of talin processing. Furthermore, CyaA mutants unable to mobilize calcium into cells failed to relocate into lipid rafts, and failed to translocate the AC domain across cell membrane, unless rescued by Ca(2+) influx promoted in trans by ionomycin or another CyaA protein. Hence, by mobilizing calcium ions into phagocytes, the 'translocation intermediate' promotes toxin piggybacking on integrin into lipid rafts and enables AC enzyme delivery into host cytosol.
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