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

Koutaro Ishibashi, Takefumi Uemura, Satoshi Waguri, Mitsunori Fukuda

    Research output: Contribution to journalArticle

    38 Citations (Scopus)

    Abstract

    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.

    Original languageEnglish
    Pages (from-to)3193-3202
    Number of pages10
    JournalMolecular biology of the cell
    Volume23
    Issue number16
    DOIs
    Publication statusPublished - 2012 Aug

    ASJC Scopus subject areas

    • Molecular Biology
    • Cell Biology

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