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Full length RTN3 regulates turnover of tubular endoplasmic reticulum via selective autophagy

Type of publication Peer-reviewed
Publikationsform Original article (peer-reviewed)
Author Grumati Paolo, Morozzi Giulio, Hölper Soraya, Mari Muriel, Harwardt Marie-Lena IE, Yan Riqiang, Müller Stefan, Reggiori Fulvio, Heilemann Mike, Dikic Ivan,
Project ER-phagy mechanisms to maintain and restore endoplasmic reticulum homeostasis
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Original article (peer-reviewed)

Journal eLife
Volume (Issue) 6
Page(s) e25555
Title of proceedings eLife
DOI 10.7554/elife.25555

Open Access

Type of Open Access Publisher (Gold Open Access)


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.