ArticleScientific reports2020
Crystal structure of the Rab33B/Atg16L1 effector complex.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- ZDHHC7-mediatedAutophagy · 2024Article
- When an underdog becomes a major player: the role of protein structural disorder in the Atg8 conjugation system.Autophagy · 2024Review
- Three-step docking by WIPI2, ATG16L1, and ATG3 delivers LC3 to the phagophore.Science advances · 2024Article
- Coiled-coil-mediated dimerization of Atg16 is required for binding to the PROPPIN Atg21.Open biology · 2023Article
- ATG16L1 adopts a dual-binding site mode to interact with WIPI2b in autophagy.Science advances · 2023Article
- Structural biology of the Atg8 and Atg12 conjugation systems.Autophagy reports · 2023Review
- LC3-associated endocytosis and the functions of Rubicon and ATG16L1.Science advances · 2022Review
- Rab33b-exocyst interaction mediates localized secretion for focal adhesion turnover and cell migration.iScience · 2022Article
- Article
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Atg12-Atg5/Atg16L1 complex is recruited by WIPI2b to the site of autophagosome formation. Atg16L1 is an effector of the Golgi resident GTPase Rab33B. Here we identified a minimal stable complex of murine Rab33B(30-202) Q92L and Atg16L1(153-210). Atg16L1(153-210) comprises the C-terminal part of the Atg16L1 coiled-coil domain. We have determined the crystal structure of the Rab33B Q92L/Atg16L1(153-210) effector complex at 3.47 Å resolution. This structure reveals that two Rab33B molecules bind to the diverging α-helices of the dimeric Atg16L1 coiled-coil domain. We mutated Atg16L1 and Rab33B interface residues and found that they disrupt complex formation in pull-down assays and cellular co-localization studies. The Rab33B binding site of Atg16L1 comprises 20 residues and immediately precedes the WIPI2b binding site. Rab33B mutations that abolish Atg16L binding also abrogate Rab33B association with the Golgi stacks. Atg16L1 mutants that are defective in Rab33B binding still co-localize with WIPI2b in vivo. The close proximity of the Rab33B and WIPI2b binding sites might facilitate the recruitment of Rab33B containing vesicles to provide a source of lipids during autophagosome biogenesis.
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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.