The ULK1 complex Sensing nutrient signals for autophagy activation

Pui-Mun Wong, Cindy Puente, Ian G. Ganley, Xuejun Jiang

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    260 Citations (Scopus)

    Abstract

    The Atg1/ULK1 complex plays a central role in starvation-induced autophagy, integrating signals from upstream sensors such as MTOR and AMPK and transducing them to the downstream autophagy pathway. Much progress has been made in the last few years in understanding the mechanisms by which the complex is regulated through protein-protein interactions and post-translational modifications, providing insights into how the cell modulates autophagy, particularly in response to nutrient status. However, how the ULK1 complex transduces upstream signals to the downstream central autophagy pathway is still unclear. Although the protein kinase activity of ULK1 is required for its autophagic function, its protein substrate(s) responsible for autophagy activation has not been identified. Furthermore, examples of potential ULK1-independent autophagy have emerged, indicating that under certain specific contexts, the ULK1 complex might be dispensable for autophagy activation. This raises the question of how the autophagic machinery is activated independent of the ULK1 complex and what are the biological functions of such noncanonical autophagy pathways.

    Original languageEnglish
    Pages (from-to)124-137
    Number of pages14
    JournalAutophagy
    Volume9
    Issue number2
    DOIs
    Publication statusPublished - 2013

    Keywords

    • INDEPENDENTLY TARGET
    • C-ELEGANS
    • AXONAL ELONGATION
    • AMPK
    • Atg1
    • kinase
    • CAENORHABDITIS-ELEGANS
    • UNC-51-LIKE KINASE
    • regulation
    • SERINE/THREONINE KINASE
    • MTOR
    • PROTEIN-KINASE COMPLEX
    • NONAPOPTOTIC CELL-DEATH
    • SACCHAROMYCES-CEREVISIAE
    • ATG1 KINASE

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