Autophagy-independent LC3 function in vesicular traffic

被引：29

作者：

de Haan, Cornelis A. M. ^{[3
]}

Molinari, Maurizio ^{[4
,5
]}

Reggiori, Fulvio ^{[1
,2
]}

机构：

[1] Univ Med Ctr Utrecht, Dept Cell Biol, Utrecht, Netherlands

[2] Univ Med Ctr Utrecht, Inst Biomembranes, Utrecht, Netherlands

[3] Univ Utrecht, Div Virol, Dept Infect Dis & Immunol, Utrecht, Netherlands

[4] Biomed Res Inst, Bellinzona, Switzerland

[5] Ecole Polytech Fed Lausanne, Sch Life Sci, Lausanne, Switzerland

来源：

AUTOPHAGY | 2010年 / 6卷 / 07期

关键词：

LC3-I; EDEMosomes; ERAD tuning; double-membrane vesicles; coronavirus; autophagy;

D O I：

10.4161/auto.6.7.13309

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

As protein folding is an imperfect process, the endoplasmic reticulum (ER) contains folding as well as ER-associated degradation (ERAD) machineries. In order to prevent premature interruption of folding, ERAD regulators and effectors such as EDEM1 and OS-9 are selectively cleared from the ER in so-called EDEMosomes to down-regulate the degradative activity. The mechanism by which EDEM1 and OS-9 are subjected to rapid turnover, also known as ERAD tuning, shows similarities with, but is clearly distinct from, macroautophagy. Positive strand RNA coronaviruses (CoVs) such as the severe acute respiratory syndrome (SARS)-CoV and mouse hepatitis virus (MHV), induce in infected cells the formation of autophagosome-like, double-membrane vesicles (DMVs) to which their replication and transcription complexes are anchored. While it seems clear that CoVs hijack ER-derived host cell membranes for replication, the mechanism by which these DMVs are assembled has remained completely mysterious.

引用

页码：994 / 996

页数：3