Control of GABARAP‐mediated autophagy by the Golgi complex, centrosome and centriolar satellites. (27th October 2017)

• Record Type: Journal Article
• Authors: Joachim, Justin; Tooze, Sharon A.
• Is Part Of: Biology of the cell. Volume 110:Number 1(2018)
• Page Start: 1
• Page End: 5
• Publication Date: 2017-10-27
• Subjects: Autophagosome -- GOLGA2 -- PCM1 -- Phagophore -- WAC; Cytology -- Periodicals; Electron microscopy -- Periodicals; 571.6
• DOI: 10.1111/boc.201700046
• Languages: English
• ISSNs: 0248-4900

Abstract

Abstract: Within minutes of induction of autophagy by amino‐acid starvation in mammalian cells, multiple autophagosomes form throughout the cell cytoplasm. During their formation, the autophagosomes sequester cytoplasmic material and deliver it to lysosomes for degradation. How these organelles can be so rapidly formed and how their formation is acutely regulated are major questions in the autophagy field. Protein and lipid trafficking from diverse cell compartments contribute membrane to, or regulate the formation of the autophagosome. In addition, recruitment of Atg8 (in yeast), and the ATG8‐family members (in mammalian cells) to autophagosomes is required for efficient autophagy. Recently, it was discovered that the centrosome and centriolar satellites regulate autophagosome formation by delivery of an ATG8‐family member, GABARAP, to the forming autophagosome membrane, the phagophore. We propose that GABARAP regulates phagophore expansion by activating the ULK complex, the amino‐acid controlled initiator complex. This finding reveals a previously unknown link between the centrosome, centriolar satellites and autophagy. Abstract : Review : Autophagosome formation is a complex process. In addition to the known function of membrane‐bound organelles, a role for the centrosome and centriolar satellites has been discovered. The dynamic transport of GABARAP (GABA) from the centrosome to the forming autophagosome, the phagophore, provides a new pathway and regulatory link to control the formation of autophagosomes.