ArticleAutophagy2024
PtdIns4P is required for the autophagosomal recruitment of STX17 (syntaxin 17) to promote lysosomal fusion.
Article in Autophagy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 14 citations in OpenAlex.
- Regulation and roles of mammalian mitophagy.Nature reviews. Molecular cell biology · 2026Review
- Targeting VAMPs in Aging-Related Diseases: From Mechanisms to Pharmacotherapy.Pharmaceutical research · 2026Review
- Acetylation of STX17 promotes its autophagosomal translocation.Nature communications · 2026Article
- Review
- MCOLN1/TRPML1-MCOLN3/TRPML3 heteromer and its coupling to CaAutophagy · 2025Article
- Lysosome heterogeneity and diversity mapped through its distinct cellular functions.Cellular and molecular life sciences : CMLS · 2025Review
- Temporally integrated multiomics analysis elucidates intricate regulatory mechanisms of ASFV in a wild boar lung-derived clonal cell line.Veterinary research · 2025Article
- Spatio-temporal processes in autophagosome-lysosome fusion.Medical review (2021) · 2025Review
- HOPS-dependent vesicle tethering lock inhibits endolysosomal fusions and autophagosome secretion upon the loss of Syntaxin17.Science advances · 2025Article
- Autophagosomes coated in situ with nanodots act as personalized cancer vaccines.Nature nanotechnology · 2025Article
- Identification of the GABARAP binding determinant in PI4K2A.Bioscience reports · 2024Article
- Syntaxin 17 recruitment to mature autophagosomes is temporally regulated by PI4P accumulation.eLife · 2024Article
- A matter of timing.eLife · 2024Article
- Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The autophagosomal SNARE STX17 (syntaxin 17) promotes lysosomal fusion and degradation, but its autophagosomal recruitment is incompletely understood. Notably, PtdIns4P is generated on autophagosomes and promotes fusion through an unknown mechanism. Here we show that soluble recombinant STX17 is spontaneously recruited to negatively charged liposomes and adding PtdIns4P to liposomes containing neutral lipids is sufficient for its recruitment. Consistently, STX17 colocalizes with PtdIns4P-positive autophagosomes in cells, and specific inhibition of PtdIns4P synthesis on autophagosomes prevents its loading. Molecular dynamics simulations indicate that C-terminal positively charged amino acids establish contact with membrane bilayers containing negatively charged PtdIns4P. Accordingly, Ala substitution of Lys and Arg residues in the C terminus of STX17 abolishes membrane binding and impairs its autophagosomal recruitment. Finally, only wild type but not Ala substituted STX17 expression rescues the autophagosome-lysosome fusion defect of STX17 loss-of-function cells. We thus identify a key step of autophagosome maturation that promotes lysosomal fusion.
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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.