ERAD and protein import defects in a sec61 mutant lacking ER-lumenal loop 7.

ABSTRACT:

Background

The Sec61 channel mediates protein translocation across the endoplasmic reticulum (ER) membrane during secretory protein biogenesis, and likely also during export of misfolded proteins for ER-associated degradation (ERAD). The mechanisms of channel opening for the different modes of translocation are not understood so far, but the position of the large ER-lumenal loop 7 of Sec61p suggests a decisive role.

Results

We show here that the Y345H mutation in L7 which causes diabetes in the mouse displays no ER import defects in yeast, but a delay in misfolded protein export. A complete deletion of L7 in Sec61p resulted in viable, cold- and tunicamycin-hypersensitive yeast cells with strong defects in posttranslational protein import of soluble proteins into the ER, and

SUBMITTER: Tretter T 

PROVIDER: S-EPMC3897919 | biostudies-literature | 2013 Dec

REPOSITORIES: biostudies-literature