Autophagy articles within Nature

Featured

  • Perspective |

    The mechanisms by which mitochondria are transferred between cells and how intercellular mitochondria transfer regulates physiological processes and disease pathogenesis are discussed.

    • Nicholas Borcherding
    •  & Jonathan R. Brestoff
  • Article
    | Open Access

    A proteomics analysis demonstrates that, during nutrient stress, mammalian cells prioritize degradation by autophagy of membrane proteins and identifies receptors that mediate this process at the Golgi and also have a role in Golgi remodelling during neuronal differentiation.

    • Kelsey L. Hickey
    • , Sharan Swarup
    •  & J. Wade Harper
  • Article
    | Open Access

    Insect salivary protein (BISP) targets OsRLCK185 to suppress defence in susceptible plants, whereas in resistant plants BISP binds BPH14 to activate host plant resistance. To restore cellular homeostasis, the resistance mechanism is fine-tuned by selective autophagy.

    • Jianping Guo
    • , Huiying Wang
    •  & Guangcun He
  • Article
    | Open Access

    The membrane-shaping protein ARL6IP1 is involved in the selective degradation of the endoplasmic reticulum, and this process depends on its ubiquitination and interaction with other membrane-shaping proteins such as FAM134B.

    • Hector Foronda
    • , Yangxue Fu
    •  & Christian A. Hübner
  • Article |

    Unphosphorylated PINK1 of Pediculus humanus corporis forms a dimerized state before undergoing trans-autophosphorylation, and phosphorylated PINK1 undergoes a conformational change in the N-lobe to produce its phosphorylated, ubiquitin-binding state.

    • Zhong Yan Gan
    • , Sylvie Callegari
    •  & David Komander
  • Article |

    Upon Salmonella invasion of the mammalian cytosol, ubiquitylation of a non-proteinaceous substrate—the lipid A moiety of bacterial lipopolysaccharide—by the E3 ubiquitin ligase RNF213 marks the bacteria as cargo for antibacterial autophagy.

    • Elsje G. Otten
    • , Emma Werner
    •  & Felix Randow
  • Article |

    A theoretical model, in vitro reconstitution and in vivo experimentation show that competition between droplet surface tension and membrane sheet instability dictates the form and function of autophagosomal membranes.

    • Jaime Agudo-Canalejo
    • , Sebastian W. Schultz
    •  & Roland L. Knorr
  • Article |

    Genome-wide siRNA screens identify an essential function for sorting nexin 5 in virus-induced autophagy and immunity mediated via class III phosphatidylinositol-3-kinase complex 1.

    • Xiaonan Dong
    • , Yuting Yang
    •  & Beth Levine
  • Article |

    In-cell structural studies in Saccharomyces cerevisiae reveal that the configuration of the Nup159 complex is a key determinant of the mRNA export function of the nuclear pore complex, and suggest a model in which nuclear pore complexes are degraded via the autophagy machinery.

    • Matteo Allegretti
    • , Christian E. Zimmerli
    •  & Martin Beck
  • Article |

    During nutrient stress, ribosomal protein abundance is regulated primarily by translational and non-autophagic degradative mechanisms, but ribosome density per cell is largely maintained by reductions in cell volume and rates of cell division.

    • Heeseon An
    • , Alban Ordureau
    •  & J. Wade Harper
  • Article |

    Compounds that interact with mutant huntingtin and an autophagosomal protein are able to reduce cellular levels of mutant huntingtin by targeting it for autophagic degradation, demonstrating an approach that may have potential for treating proteopathies.

    • Zhaoyang Li
    • , Cen Wang
    •  & Boxun Lu
  • Letter |

    Phosphorylation of one of two adjacent serine residues in TSC2 is both required and sufficient for PKG1-mediated cardiac protection against pressure overload in mice; these serine residues provide a genetic tool for the bidirectional regulation of stress-stimulated mTORC1 activity.

    • Mark J. Ranek
    • , Kristen M. Kokkonen-Simon
    •  & David A. Kass
  • Letter |

    Mice with whole-body or liver-specific deletion of Atg7 release circulating arginase I and have reduced levels of serum arginine, which impairs the growth of allografted arginine-auxotrophic tumours.

    • Laura Poillet-Perez
    • , Xiaoqi Xie
    •  & Eileen White
  • Letter |

    The polyglutamine domain in ataxin 3, which is expanded in spinocerebellar ataxia type 3, allows normal ataxin 3 to interact with and deubiquitinate beclin 1 and thereby to promote autophagy.

    • Avraham Ashkenazi
    • , Carla F. Bento
    •  & David C. Rubinsztein
  • Letter |

    During early-stage tumour growth in Drosphila, tumour cells acquire necessary nutrients by triggering autophagy in surrounding cells in the tumour microenvironment.

    • Nadja S. Katheder
    • , Rojyar Khezri
    •  & Tor Erik Rusten
  • Letter |

    An investigation into the nuclear events involved in autophagy regulation identifies the histone arginine methyltransferase CARM1 as a transcriptional co-activator of transcription factor TFEB; CARM1 levels are decreased by the SKP2-containing E3 ubiquitin ligase and increased during autophagy induction after nutrient starvation.

    • Hi-Jai R. Shin
    • , Hyunkyung Kim
    •  & Sung Hee Baek
  • Article |

    The regenerative properties of muscle stem cells decline with age as the stem cells enter an irreversible state of senescence; a study of mouse muscle stem cells reveals that entry into senescence is an autophagy-dependent process and promoting autophagy in old satellite cells can reverse senescence and restore their regenerative properties in an injury model.

    • Laura García-Prat
    • , Marta Martínez-Vicente
    •  & Pura Muñoz-Cánoves
  • Letter |

    During postnatal development in mice, the growth factor FGF18 induces autophagy in the chondrocyte cells of the growth plate to regulate the secretion of type II collagen, a process required for bone growth.

    • Laura Cinque
    • , Alison Forrester
    •  & Carmine Settembre
  • Letter |

    In response to cancer-associated stress, autophagy machinery mediates degradation of nuclear lamina components in mammals, suggesting that cells might degrade nuclear components to prevent tumorigenesis.

    • Zhixun Dou
    • , Caiyue Xu
    •  & Shelley L. Berger
  • Article |

    The PINK1 ubiquitin kinase is shown to recruit the two autophagy receptors NDP52 and OPTN to mitochondria to activate mitophagy directly, independently of the ubiquitin ligase parkin; once recruited to mitochondria, NDP52 and OPTN recruit autophagy initiation components, and parkin may amplify the phospho-ubiquitin signal generated by PINK1, resulting in robust autophagy induction.

    • Michael Lazarou
    • , Danielle A. Sliter
    •  & Richard J. Youle
  • Letter |

    In yeast, the novel protein Atg40 is enriched in the cortical and cytoplasmic endoplasmic reticulum (ER), and loads these ER subdomains into autophagosomes to facilitate ER autophagy; Atg39 localizes to the perinuclear ER and induces autophagic sequestration of part of the nucleus, thus ensuring cell survival under nitrogen-deprived conditions.

    • Keisuke Mochida
    • , Yu Oikawa
    •  & Hitoshi Nakatogawa
  • Letter |

    The protein FAM134B is an endoplasmic reticulum (ER)-resident receptor that facilitates ER autophagy, and downregulation of this protein (mutations of which are also known to cause sensory neuropathy in humans) results in expanded ER structures and degeneration of mouse sensory neurons.

    • Aliaksandr Khaminets
    • , Theresa Heinrich
    •  & Ivan Dikic
  • Letter |

    The FXR–CREB axis is identified as a key physiological switch that regulates autophagy during feeding/fasting cycles; in the fed state, the nuclear receptor FXR is shown to suppress autophagy in the liver by inhibiting autophagy-associated lipid breakdown triggered under fasting conditions by the transcriptional activator CREB.

    • Sunmi Seok
    • , Ting Fu
    •  & Jongsook Kim Kemper
  • Letter |

    The nuclear receptors FXR and PPARα are shown to regulate autophagy by competing for binding to shared sites in the promoters of autophagic genes; in the fed state FXR suppresses hepatic autophagy, whereas in the fasted state PPARα is activated and reverses the normal suppression of autophagy.

    • Jae Man Lee
    • , Martin Wagner
    •  & David D. Moore
  • Article |

    The Crohn’s disease risk-conferring T300A variant in the autophagy protein ATG16L1 increases its sensitivity to caspase-3-mediated cleavage; this decreases the induction of autophagy in response to metabolic stress or pathogen infection, leading to increased secretion of inflammatory cytokines.

    • Aditya Murthy
    • , Yun Li
    •  & Menno van Lookeren Campagne
  • Letter |

    Mitophagy is the elimination of damaged mitochondria by the autophagosome regulated by the ubiquitin ligase, parkin and the kinase PINK1; a genome-wide RNAi screen with high-content microscopy has identified new genes that have an upstream role in parkin translocation to the mitochondria.

    • Samuel A. Hasson
    • , Lesley A. Kane
    •  & Richard J. Youle
  • Article |

    The primary cilium is a microtubule-based organelle that functions in sensory and signal transduction; here the authors show that the primary cilium is required for activation of starvation-induced autophagy and that basal autophagy negatively regulates ciliogenesis.

    • Olatz Pampliega
    • , Idil Orhon
    •  & Ana Maria Cuervo
  • Letter |

    The primary cilium is a microtubule-based organelle that functions in sensory and signal transduction; the authors demonstrate here that autophagic degradation of the oral-facial-digital syndrome 1 (OFD1) protein at centriolar satellites promotes primary cilium biogenesis, and that autophagy modulation might provide a novel means of ciliopathy treatment.

    • Zaiming Tang
    • , Mary Grace Lin
    •  & Qing Zhong
  • Letter |

    This study shows that autophagosomes form at sites of contact between the endoplasmic reticulum and mitochondria, and that formation requires the SNARE protein syntaxin 17.

    • Maho Hamasaki
    • , Nobumichi Furuta
    •  & Tamotsu Yoshimori
  • Article |

    A cell-permeable peptide is constructed that is derived from a region of an essential autophagy protein called beclin 1; the peptide is a potent inducer of autophagy in mammalian cells and in vivo in mice, and is effective in the clearance of several viruses.

    • Sanae Shoji-Kawata
    • , Rhea Sumpter
    •  & Beth Levine