TY  - JOUR
A1  - Grumati, Paolo
A1  - Morozzi, Giulio
A1  - Hölper, Soraya
A1  - Mari, Muriel
A1  - Harwardt, Marie-Lena I. E.
A1  - Yan, Riqiang
A1  - Müller, Stefan
A1  - Reggiori, Fulvio
A1  - Heilemann, Mike
A1  - Đikić, Ivan
T1  - Full length RTN3 regulates turnover of tubular endoplasmic reticulum via selective autophagy
T2  - eLife
N2  - The turnover of endoplasmic reticulum (ER) ensures the correct biological activity of its distinct domains. In mammalian cells, the ER is degraded via a selective autophagy pathway (ER-phagy), mediated by two specific receptors: FAM134B, responsible for the turnover of ER sheets and SEC62 that regulates ER recovery following stress. Here, we identified reticulon 3 (RTN3) as a specific receptor for the degradation of ER tubules. Oligomerization of the long isoform of RTN3 is sufficient to trigger fragmentation of ER tubules. The long N-terminal region of RTN3 contains several newly identified LC3-interacting regions (LIR). Binding to LC3s/GABARAPs is essential for the fragmentation of ER tubules and their delivery to lysosomes. RTN3-mediated ER-phagy requires conventional autophagy components, but is independent of FAM134B. None of the other reticulon family members have the ability to induce fragmentation of ER tubules during starvation. Therefore, we assign a unique function to RTN3 during autophagy.
KW  - Research article
KW  - Biochemistry
KW  - Cell biology
KW  - Selective autophagy
KW  - Endoplasmic reticulum
KW  - Rtn3
KW  - Reticulon
KW  - Autophagy
Y1  - 2017
UR  - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/44709
UR  - https://nbn-resolving.org/urn:nbn:de:hebis:30:3-447092
SN  - 2050-084X
N1  - Copyright Grumati et al. This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.
VL  - 6
IS  - e25555
SP  - 1
EP  - 32
PB  - eLife Sciences Publications
CY  - Cambridge
ER  -