Atg16L1 Protein Regulates Hormone Secretion Independent of Autophagy

Koutaro Ishibashi, Mitsunori Fukuda

    Research output: Chapter in Book/Report/Conference proceedingChapter


    Atg16L1 is an essential factor for canonical autophagy, a conserved bulk degradation system in all eukaryotes. Atg16L1 forms a complex with Atg12-conjugated Atg5, i.e., an Atg16L1-5-12 complex, and promotes elongation of isolation membranes possibly by recruiting LC3 and by facilitating its lipidation. Because of its critical role in canonical autophagy, cells from Atg16L1-deficient mice exhibit complete loss of autophagosome formation. Interestingly, the intestinal Paneth cells of Atg16L1-deficient mice exhibit a secretion defect, but the mechanism by which Atg16L1 regulates the secretory pathway is poorly understood. We recently reported the finding that Atg16L1 localizes on hormone-containing dense-core vesicles in neuroendocrine PC12 cells independent of canonical autophagy and that small GTPase Rab33A recruits the Atg16L1-5-12 complex to dense-core vesicles. We also found that knockdown of Atg16L1 in PC12 cells caused a dramatic reduction in hormone secretion independent of the autophagic activity of the cells. Our findings indicate that, in addition to its role in autophagy, Atg16L1 (or the Atg16L1-5-12 complex) regulates hormone secretion from dense-core vesicles, most likely by acting as a Rab33A effector in particular cell types, including PC12 cells.

    Original languageEnglish
    Title of host publicationRole of Autophagy in Therapeutic Applications
    PublisherElsevier Inc.
    Number of pages11
    ISBN (Electronic)9780128010525
    ISBN (Print)9780128010433
    Publication statusPublished - 2015 Feb 18


    • Atg16L1
    • Atg16L1-5-12 complex
    • Autophagy
    • Canonical autophagy
    • Crohn's disease

    ASJC Scopus subject areas

    • Immunology and Microbiology(all)


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