Series |

Series on Autophagy

Autophagy is a catabolic process through which cells replenish their macromolecular stores in response to nutrient deficiency, and also maintain homeostatic health and survival by degrading damaged proteins and organelles. Autophagy has emerged as a fundamental and conserved cellular mechanism with complex roles in health and disease. Nature Cell Biology presents a series of specially commissioned articles that will discuss recent advances and outstanding questions driving this expanding and diverse field. An accompanying online library contains research and Review articles on this topic published in the past two years by Nature Cell Biology and the Nature journals.

Series Content

  • Nature Cell Biology | Review Article

    In this Review Article, Klionsky and co-authors discuss selective autophagy pathways that degrade unwanted cytosolic components and organelles, and how these pathways require ligand receptors and scaffold proteins for cargo specificity.

    • Damián Gatica
    • , Vikramjit Lahiri
    •  &  Daniel J. Klionsky
  • Nature Cell Biology | Review Article

    Autophagy and cancer: In this Review, Galluzzi and colleagues discuss the cellular and molecular mechanisms whereby autophagy functions in multiple aspects of malignant disease, including cancer initiation, progression and responses to therapy.

    • Marissa D. Rybstein
    • , José Manuel Bravo-San Pedro
    • , Guido Kroemer
    •  &  Lorenzo Galluzzi
  • Nature Cell Biology | Review Article

    In this Review, Tavernarakis and colleagues describe recent advances in delineating the molecular mechanisms that mediate mitophagy, and discuss the complex roles of this pathway in physiological and pathological contexts.

    • Konstantinos Palikaras
    • , Eirini Lionaki
    •  &  Nektarios Tavernarakis
  • Nature Cell Biology | Review Article

    In this Review, Doherty and Baehrecke discuss the multiple roles of autophagy during cell survival and cell death. They cover the interplay between autophagy, apoptosis and necrosis, as well as engulfment and inflammation.

    • Johnna Doherty
    •  &  Eric H. Baehrecke
  • Nature Cell Biology | Review Article

    In this Review, Leidal et al. discuss the role and regulation of autophagy in aging. They cover how autophagy promotes longevity and restricts cellular damage, and discuss autophagy modulators for the potential treatment of age-related diseases.

    • Andrew M. Leidal
    • , Beth Levine
    •  &  Jayanta Debnath

Editorial & Research Highlights

  • Nature Cell Biology | Editorial

    Autophagy is a cellular degradation and recycling process with complex roles in health and disease and emerging relevance to translational research. In this issue, we launch a Series of commissioned articles that will discuss recent advances and outstanding questions driving this rapidly expanding and diverse field.

Related Nature Cell Biology Research

  • Nature Cell Biology | News & Views

    Selective autophagy is important for controlled degradation of cellular components. However, a selective autophagic degradation mechanism for ribosomes in mammals has remained unclear. A study now describes non-selective and selective ribosome degradation and a significant role for ‘bystander’ non-selective autophagy.

    • Christian Münch
    •  &  Ivan Dikic
  • Nature Cell Biology | Article

    Fumagalli et al. show that Sec62 delivers ER components to the autolysosome for clearance by acting as a receptor for autophagy protein LC3-II. This identifies Sec62 as a critical factor for selective ER turnover.

    • Fiorenza Fumagalli
    • , Julia Noack
    • , Timothy J. Bergmann
    • , Eduardo Cebollero
    • , Giorgia Brambilla Pisoni
    • , Elisa Fasana
    • , Ilaria Fregno
    • , Carmela Galli
    • , Marisa Loi
    • , Tatiana Soldà
    • , Rocco D’Antuono
    • , Andrea Raimondi
    • , Martin Jung
    • , Armin Melnyk
    • , Stefan Schorr
    • , Anne Schreiber
    • , Luca Simonelli
    • , Luca Varani
    • , Caroline Wilson-Zbinden
    • , Oliver Zerbe
    • , Kay Hofmann
    • , Matthias Peter
    • , Manfredo Quadroni
    • , Richard Zimmermann
    •  &  Maurizio Molinari
  • Nature Cell Biology | News & Views

    The endoplasmic reticulum (ER) is the largest membrane-bound organelle in cells, and its size needs to be carefully controlled. Downsizing the ER by autophagy is now shown to involve Sec62, a protein that also helps to build up the organelle. This link suggests a molecular switch for ER size control.

    • Sebastian Schuck

Related Nature Journals Research

  • Nature Immunology | Article

    The survival of hematopoietic stem cells requires tight regulation of mitophagy. Lin and colleagues show that Atad3a regulates mitophagy in these cells by sequestering the mitophagy initiator Pink1 and directing its import via the mitochondrial Tom40–Tim23 complex.

    • Guoxiang Jin
    • , Chuan Xu
    • , Xian Zhang
    • , Jie Long
    • , Abdol Hossein Rezaeian
    • , Chunfang Liu
    • , Mark E. Furth
    • , Steven Kridel
    • , Boris Pasche
    • , Xiu-Wu Bian
    •  &  Hui-Kuan Lin
  • Nature Immunology | Article

    Various intracellular pathogens attempt to hide from innate cytosolic sensors by forming vacuoles. Yamamoto and colleagues show that the autophagy-related protein Gate-16, which is induced by interferon-γ, is required for noncanonical autophagy to control infection by Toxoplasma gondii.

    • Miwa Sasai
    • , Naoya Sakaguchi
    • , Ji Su Ma
    • , Shuhei Nakamura
    • , Tsuyoshi Kawabata
    • , Hironori Bando
    • , Youngae Lee
    • , Tatsuya Saitoh
    • , Shizuo Akira
    • , Akiko Iwasaki
    • , Daron M Standley
    • , Tamotsu Yoshimori
    •  &  Masahiro Yamamoto
  • Nature Communications | Article | open

    Soluble misfolded proteins that fail to be degraded by the ubiquitin proteasome system (UPS) are redirected to autophagy via specific adaptors, such as p62. Here the authors show that p62 recognises N-degrons in these proteins, acting as a N-recognin from the proteolytic N-end rule pathway, and targets these cargos to autophagosomal degradation.

    • Hyunjoo Cha-Molstad
    • , Ji Eun Yu
    • , Zhiwei Feng
    • , Su Hyun Lee
    • , Jung Gi Kim
    • , Peng Yang
    • , Bitnara Han
    • , Ki Woon Sung
    • , Young Dong Yoo
    • , Joonsung Hwang
    • , Terry McGuire
    • , Sang Mi Shim
    • , Hyun Dong Song
    • , Srinivasrao Ganipisetti
    • , Nuozhou Wang
    • , Jun Min Jang
    • , Min Jae Lee
    • , Seung Jun Kim
    • , Kyung Ho Lee
    • , Jin Tae Hong
    • , Aaron Ciechanover
    • , Inhee Mook-Jung
    • , Kwang Pyo Kim
    • , Xiang-Qun Xie
    • , Yong Tae Kwon
    •  &  Bo Yeon Kim
  • Nature Communications | Article | open

    During autophagy, AMPK and mTOR associate with ULK1 and regulate phosphatidylinositol 3-phosphate (PtdIns3P) production that mediates autophagosome formation via WIPI proteins. Here the authors show WIPI3 and WIPI4 have a scaffolding function upstream of PtdIns3P production and have a role in the PtdIns3P effector function of WIPI1-WIPI2 at nascent autophagosomes.

    • Daniela Bakula
    • , Amelie J. Müller
    • , Theresia Zuleger
    • , Zsuzsanna Takacs
    • , Mirita Franz-Wachtel
    • , Ann-Katrin Thost
    • , Daniel Brigger
    • , Mario P. Tschan
    • , Tancred Frickey
    • , Horst Robenek
    • , Boris Macek
    •  &  Tassula Proikas-Cezanne
  • Nature | News & Views

    Mutant proteins that contain stretches called polyQ repeats can misfold or form aggregates linked to neurodegeneration. It emerges that some polyQ-containing proteins regulate a process that degrades misfolded proteins. See Letter p.108

    • Dale D. O. Martin
    •  &  Michael R. Hayden
  • Nature | 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
    • , Thomas Ricketts
    • , Mariella Vicinanza
    • , Farah Siddiqi
    • , Mariana Pavel
    • , Ferdinando Squitieri
    • , Maarten C. Hardenberg
    • , Sara Imarisio
    • , Fiona M. Menzies
    •  &  David C. Rubinsztein