4.4 Article

Atg16L1, an essential factor for canonical autophagy, participates in hormone secretion from PC12 cells independently of autophagic activity

Journal

MOLECULAR BIOLOGY OF THE CELL
Volume 23, Issue 16, Pages 3193-3202

Publisher

AMER SOC CELL BIOLOGY
DOI: 10.1091/mbc.E12-01-0010

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Funding

  1. Ministry of Education, Culture, Sports, and Technology of Japan
  2. Global COE Program (Basic and Translational Research Center for Global Brain Science) of the Ministry of Education, Culture, Sports, and Technology of Japan
  3. Japan Society for the Promotion of Science
  4. Grants-in-Aid for Scientific Research [24390048, 20113006] Funding Source: KAKEN

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Autophagy is a bulk degradation system in all eukaryotic cells and regulates a variety of biological activities in higher eukaryotes. Recently involvement of autophagy in the regulation of the secretory pathway has also been reported, but the molecular mechanism linking autophagy with the secretory pathway remains largely unknown. Here we show that Atg16L1, an essential protein for canonical autophagy, is localized on hormone-containing dense-core vesicles in neuroendocrine PC12 cells and that knockdown of Atg16L1 causes a dramatic reduction in the level of hormone secretion independently of autophagic activity. We also find that Atg16L1 interacts with the small GTPase Rab33A and that this interaction is required for the dense-core vesicle localization of Atg16L1 in PC12 cells. Our findings indicate that Atg16L1 regulates not only autophagy in all cell types, but also secretion from dense-core vesicles, presumably by acting as a Rab33A effector, in particular cell types.

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