Authors: Justin Joachim, Martina Wirth, Nicole C. McKnight and Sharon A. Tooze

Justin Joachim

London Research Institute; Cancer Research UK; London, UK
These authors contributed equally to this work.

Martina Wirth

London Research Institute; Cancer Research UK; London, UK
These authors contributed equally to this work.

Nicole C. McKnight

Department of Neurology; Friedman Brain Institute; Mount Sinai School of Medicine New York, NY USA

Sharon A. Tooze

Corresponding author: sharon.tooze@cancer.org.uk
London Research Institute; Cancer Research UK; London, UK

Abstract:
Autophagy is a conserved and highly regulated catabolic pathway, transferring cytoplasmic components in autophagosomes to lysosomes for degradation and providing amino acids during starvation. In multicellular organisms autophagy plays an important role for tissue homeostasis, and deregulation of autophagy has been implicated in a broad range of diseases, including cancer and neurodegenerative disorders. In mammals, many aspects of autophagy still need to be fully elucidated: what is the exact hierarchy and relationship between ATG proteins and other factors that lead to the formation and expansion of phagophores? Where does the membrane source for autophagosome formation originate? Which signaling events trigger amino acid starvation-induced autophagy? How are the activities of ULK1/2 and the class III PtdIns3K regulated and linked to each other? To develop therapeutic strategies to manipulate autophagy in human disease, a comprehensive understanding of the molecular protein machinery mediating and regulating autophagy is required.

Autophagic Punctum to:
NC McKnight, HBJ Jefferies, EA Alemu, RE Saunders, M Howell, T Johansen, et al. Genome-wide siRNA screen reveals amino acid starvation-induced autophagy requires SCOC and WAC. EMBO J 2012; 31: 1931-46
PMID: 22354037 DOI: 10.1038/emboj.2012.36

Received: June 1, 2012; Accepted: June 6, 2012; Published Online: June 21, 2012

Preview: