ArticleThe Journal of cell biology2022
V. cholerae MakA is a cholesterol-binding pore-forming toxin that induces non-canonical autophagy.
Article in The Journal of cell biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Cryo-EM structure of detergent-boundbioRxiv : the preprint server for biology · 2026Article
- The ATG8 E3-like ligases sense lysosomal damage and initiate ESCRT-mediated membrane repair.The EMBO journal · 2026Article
- Membrane microdomains are crucial forScience advances · 2026Article
- TseCurrent research in microbial sciences · 2026Article
- Pore Formation by Pore Forming Proteins in Lipid Membranes: Structural Insights Through Cryo-EM.The Journal of membrane biology · 2025Review
- The spectrum of lysosomal stress and damage responses: from mechanosensing to inflammation.EMBO reports · 2025Review
- Single-cell RNA-seq reveals a key role forFrontiers in microbiology · 2025Article
- Conjugation of ATG8s to single membranes at a glance.Journal of cell science · 2024Review
- A chemical inhibitor of IST1-CHMP1B interaction impairs endosomal recycling and induces noncanonical LC3 lipidation.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Breaking the cellular defense: the role of autophagy evasion inFrontiers in cellular and infection microbiology · 2024Article
- Article
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pore-forming toxins (PFTs) are important virulence factors produced by many pathogenic bacteria. Here, we show that the Vibrio cholerae toxin MakA is a novel cholesterol-binding PFT that induces non-canonical autophagy in a pH-dependent manner. MakA specifically binds to cholesterol on the membrane at pH < 7. Cholesterol-binding leads to oligomerization of MakA on the membrane and pore formation at pH 5.5. Unlike other cholesterol-dependent cytolysins (CDCs) which bind cholesterol through a conserved cholesterol-binding motif (Thr-Leu pair), MakA contains an Ile-Ile pair that is essential for MakA-cholesterol interaction. Following internalization, endosomal acidification triggers MakA pore-assembly followed by ESCRT-mediated membrane repair and V-ATPase-dependent unconventional LC3 lipidation on the damaged endolysosomal membranes. These findings characterize a new cholesterol-binding toxin that forms pores in a pH-dependent manner and reveals the molecular mechanism of host autophagy manipulation.
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