Ubiquilins accelerate autophagosome maturation and promote cell survival during nutrient starvation

Autophagy. 2009 May;5(4):573-5. doi: 10.4161/auto.5.4.8312.

Abstract

Ubiquilins (UBQLN), a family of adaptor proteins with partial homology with ubiquitin, are proposed to facilitate proteasomal degradation of ubiquitinated substrates. We now demonstrate a novel role for UBQLN in promoting autophagosome maturation during nutrient deprivation. Ectopic expression of UBQLN protects cells against starvation-induced cell death, while depletion renders cells more susceptible. This protective function requires the essential autophagy regulators, Atg5 and Atg7. The ubiquitin-associated (UBA) domain of UBQLN is required for its association with autophagosomes as well as for its prosurvival functions.Remarkably, during starvation-induced autophagy, UBQLN promotes the fusion of early autophagosomes with lysosomes.Overall, this work illustrates an important function for UBQLN in cell survival during nutrient starvation, which requires a newly recognized function for UBQLN in autophagosome maturation.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Carrier Proteins / metabolism*
  • Cell Survival
  • Food*
  • HeLa Cells
  • Humans
  • Lysosomes / metabolism
  • Phagosomes / metabolism*

Substances

  • Carrier Proteins