Autophagy articles within Nature

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  • News & Views |

    Cells can destroy invading bacteria through a digestive process called autophagy. A study finds that sugar molecules, exposed by bacterial damage to the cell's membrane, can trigger this process. See Letter p.414

    • Ju Huang
    •  & John H. Brumell

  • News & Views |

    The protein Sae2 mediates the repair of double-strand breaks in DNA. It emerges that Sae2 activity is controlled by both its modification with acetyl groups and its degradation by the process of autophagy. See Article p.74

    • Catherine J. Potenski
    •  & Hannah L. Klein

  • Article |

    The presence of DNA lesions is a clear signal that initiates the DNA damage response; however, the mechanisms that attenuate this response when repair has occurred are less clear. Here, deacetylation of Sae2 by Rpd3 and Hda1 is shown to be required for it to act on Mre11. When the role of Sae2 in resection is completed, it is acetylated by Gcn5 and degraded through an autophagic pathway. This work highlights links between DNA damage signalling, acetylation of repair factors, and autophagy mediated degradation of these factors.

    • Thomas Robert
    • , Fabio Vanoli
    •  & Marco Foiani

  • News & Views |

    Autophagy is an essential cellular process for protein and organelle quality control. Analyses of proteins that interact with the human autophagic machinery provide an outline of the molecular organization of this pathway.

    • Beth Levine
    •  & Rama Ranganathan

  • Article |

    Autophagy is a cellular process by which proteins and organelles are sequestered in autophagosomal vesicles and delivered to the lysosome for degradation. Here the authors present a proteomic analysis of the autophagy interaction network in human cells. Their results reveal a network of signalling modules and extensive connectivity among subnetworks. This global view of the mammalian autophagy pathway will be an important resource for future mechanistic understanding of this pathway.

    • Christian Behrends
    • , Mathew E. Sowa
    •  & J. Wade Harper

  • Letter |

    When cells are starved, the enzyme TOR is inhibited, inducing autophagy. In this process, autophagosomes sequester intracellular components and then fuse with lysosomes, producing autolysosomes in which cargo is degraded to regenerate nutrients. Now, a mechanism is revealed by which lysosomes are re-formed. When starvation conditions are prolonged, mTOR is re-activated; this attenuates autophagy and results in tubules and vesicles extruding from the autolysosome and maturing into functional lysosomes.

    • Li Yu
    • , Christina K. McPhee
    •  & Michael J. Lenardo

  • News & Views |

    Defects in mitochondria are implicated in Parkinson's disease. Study of a quality-control pathway involving the proteins PINK1 and Parkin provides further clues about the mechanism involved.

    • Asa Abeliovich

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