ArticlePLoS genetics2018
Non-canonical role of the SNARE protein Ykt6 in autophagosome-lysosome fusion.
Article in PLoS genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 102 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- SNX-3 confers lysosomal fusion-competence to sustain basal autophagy.Cellular and molecular life sciences : CMLS · 2026Article
- Multilayered interplay between the cGAS-STING pathway and autophagy.Autophagy reports · 2026Review
- Autophagy inhibition in intestinal stem cells favors enteroendocrine cell differentiation through Stat92E activity.Disease models & mechanisms · 2025Article
- Lysosome heterogeneity and diversity mapped through its distinct cellular functions.Cellular and molecular life sciences : CMLS · 2025Review
- 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
- Deacetylated SNAP47 recruits HOPS to facilitate autophagosome-lysosome fusion independent of STX17.Nature communications · 2025Article
- Virus infection and vesicle trafficking.Frontiers in immunology · 2025Review
- Mechanisms and roles of membrane-anchored ATG8s.Frontiers in cell and developmental biology · 2025Review
- Pan-Cancer Analysis Identifies YKT6 as a Prognostic and Immunotherapy Biomarker, with an Emphasis on Cervical Cancer.OncoTargets and therapy · 2025Article
- Migfilin promotes autophagic flux through direct interaction with SNAP29 and Vamp8.The Journal of cell biology · 2024Article
- Homozygous missense variants in YKT6 result in loss of function and are associated with developmental delay, with or without severe infantile liver disease and risk for hepatocellular carcinoma.Genetics in medicine : official journal of the American College of Medical Genetics · 2024Article
- Recent progresses in the late stages of autophagy.Cell insight · 2024Review
- Rab32 family proteins regulate autophagosomal components recycling.The Journal of cell biology · 2024Article
- Loss of the HOPS complex disrupts early-to-late endosome transition, impairs endosomal recycling and induces accumulation of amphisomes.Molecular biology of the cell · 2024Article
- The Ykt6-Snap29-Syx13 SNARE complex promotes crinophagy via secretory granule fusion with Lamp1 carrier vesicles.Scientific reports · 2024Article
- The STX17-SNAP47-VAMP7/VAMP8 complex is the default SNARE complex mediating autophagosome-lysosome fusion.Cell research · 2024Article
- Molecular structures and function of the autophagosome-lysosome fusion machinery.Autophagy reports · 2024Article
- The Pathological Mechanism of Neuronal Autophagy-Lysosome Dysfunction After Ischemic Stroke.Cellular and molecular neurobiology · 2023Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The autophagosomal SNARE Syntaxin17 (Syx17) forms a complex with Snap29 and Vamp7/8 to promote autophagosome-lysosome fusion via multiple interactions with the tethering complex HOPS. Here we demonstrate that, unexpectedly, one more SNARE (Ykt6) is also required for autophagosome clearance in Drosophila. We find that loss of Ykt6 leads to large-scale accumulation of autophagosomes that are unable to fuse with lysosomes to form autolysosomes. Of note, loss of Syx5, the partner of Ykt6 in ER-Golgi trafficking does not prevent autolysosome formation, pointing to a more direct role of Ykt6 in fusion. Indeed, Ykt6 localizes to lysosomes and autolysosomes, and forms a SNARE complex with Syx17 and Snap29. Interestingly, Ykt6 can be outcompeted from this SNARE complex by Vamp7, and we demonstrate that overexpression of Vamp7 rescues the fusion defect of ykt6 loss of function cells. Finally, a point mutant form with an RQ amino acid change in the zero ionic layer of Ykt6 protein that is thought to be important for fusion-competent SNARE complex assembly retains normal autophagic activity and restores full viability in mutant animals, unlike palmitoylation or farnesylation site mutant Ykt6 forms. As Ykt6 and Vamp7 are both required for autophagosome-lysosome fusion and are mutually exclusive subunits in a Syx17-Snap29 complex, these data suggest that Vamp7 is directly involved in membrane fusion and Ykt6 acts as a non-conventional, regulatory SNARE in this process.
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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 Socratic graph.