title: Ubiquilins accelerate autophagosome maturation and promote cell  survival during nutrient starvation.
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.
authors.affiliation: Macrophage Biology Laboratory, Northern California Institute for Research and Education, San Francisco, CA, USA.
authors.forename: Elsa-Noah
authors.initials: EN
authors.lastname: N'Diaye
authors.forename: Jayanta
authors.initials: J
authors.lastname: Debnath
authors.forename: Eric J
authors.initials: EJ
authors.lastname: Brown
mesh_terms: D002352:Carrier Proteins / Q000378:metabolism*; D002470:Cell Survival; D005502:Food; D006367:HeLa Cells; D006801:Humans; D008247:Lysosomes / Q000378:metabolism; D010588:Phagosomes / Q000378:metabolism*
chemical_list: D002352:Carrier Proteins