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.