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

    研究成果: Article

    38 引用 (Scopus)

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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.

    元の言語English
    ページ(範囲)3193-3202
    ページ数10
    ジャーナルMolecular biology of the cell
    23
    発行部数16
    DOI
    出版物ステータスPublished - 2012 8

    ASJC Scopus subject areas

    • Molecular Biology
    • Cell Biology

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