Sec62 regulates ER-phagy during recovery from ER stress

ABSTRACT: Perturbing ER homeostasis activates stress programs collectively called the unfolded protein response (UPR). The UPR enhances production of ER-resident chaperones and enzymes to reduce the burden of misfolded proteins. Upon resolution of ER stress, excess ER material is removed by ill-defined, selective autophagic programs. Here, using biochemical and cell-based essays, we identify a novel ER-resident autophagy receptor, Sec62, which is activated during recovery from ER stress to selectively deliver ER fragments to the autolysosomal system for clearance. Quantitative mass spectrometry analyses of autolysosomal fractions upon selective inactivation of the Sec62-regulated pathway inform on the selectivity of Sec62-regulated ER-phagy.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Permanent Cell Line Cell, Cell Culture

SUBMITTER: Manfredo Quadroni  

LAB HEAD: Maurizio Molinari

PROVIDER: PXD003961 | Pride | 2016-10-11

REPOSITORIES: Pride