ArticleNature communications2025
Molecular mechanisms of CBASS phospholipase effector CapV mediated membrane disruption.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Anti-phage defense systems in bacteria: molecular mechanisms and their role in shaping phage therapy strategies.Molecular biology reports · 2026Review
- CBASS limits bacteriophage production while maintaining cell viability in Pseudomonas aeruginosa.Cell host & microbe · 2026Article
- Crystal structure of the cytosolic Nudix-like domain of CD-NTase-associated protein 16 from Enterococcus faecalis.Acta crystallographica. Section F, Structural biology communications · 2026Article
- dITP-induced remodeling activates the filamentous effector complex in Kongming anti-phage defense.Nature communications · 2026Article
- Discovery of Small-Molecule Inhibitors of the Pycsar Antiphage Defense.ACS chemical biology · 2026Article
- Tmn blocks phage spread via plasmolysis and triggers synergistic defence responses.bioRxiv : the preprint server for biology · 2026Article
- CBASS limits bacteriophage production while maintaining cell viability inbioRxiv : the preprint server for biology · 2026Article
Corrections and comments
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Authors and funding
24 authors.
Funding
Abstract
Cyclic oligonucleotide-based antiphage signaling systems (CBASS) are widespread bacterial immune systems that trigger host suicide via cyclic nucleotide-activated effectors. The predominant strategy to induce cell death in CBASS is membrane disruption. Here, we demonstrate that patatin-like phospholipase CapV, the most abundant CBASS effector, relocates and cleaves membrane phospholipids at the cell pole upon 3'3'-cGAMP binding, inducing polarized membrane disruption and cell death. Using cryo-EM, we reveal that apo-CapV adopts both dimeric and tetrameric states, with its phospholipid-binding pocket occluded and locked in an inactive conformation. Binding to 3'3'-cGAMP induces filamentation and substantial conformational change of CapV, enhancing membrane binding via electrostatic interactions between its interspaced basic surfaces and the negatively charged phosphate moieties of phospholipids. Simultaneously, the rearrangement opens the phospholipid-binding pocket, enabling the accommodation of two fatty acid chains of phospholipid within distinct hydrophobic pockets. Our findings reveal a filament-dependent activation mechanism for phospholipase-mediated membrane disruption during antiviral response.
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