PLIC proteins or ubiquilins regulate autophagy-dependent cell survival during nutrient starvation

  • EMBO Rep. 2009 Feb;10(2):173-9. doi: 10.1038/embor.2008.238.
Elsa-Noah N'Diaye  1 ,  Kimberly K Kajihara ,  Ivy Hsieh ,  Hiroshi Morisaki ,  Jayanta Debnath ,  Eric J Brown
Affiliations
  • 1. Department of Microbial Pathogenesis, Genentech, 1 DNA Way, South San Francisco, California 94080, USA.
PMID: 19148225 DOI: 10.1038/embor.2008.238
Abstract

Ubiquilins (UBQLNs) are adaptor proteins thought to deliver ubiquitinated substrates to proteasomes. Here, we show a role for UBQLN in autophagy: enforced expression of UBQLN protects cells from starvation-induced death, whereas depletion of UBQLN renders cells more susceptible. The UBQLN protective effect requires the autophagy-related genes ATG5 and Atg7, two essential components of Autophagy. The ubiquitin-associated domain of UBQLN mediates both its association with autophagosomes and its protective effect against starvation. Depletion of UBQLN delays the delivery of autophagosomes to lysosomes. This study identifies a new role for UBQLN in regulating the maturation of Autophagy, expanding the involvement of ubiquitin-related proteins in this process.