Abstract:
:The endoplasmic reticulum (ER) is the largest intracellular endomembrane system, enabling protein and lipid synthesis, ion homeostasis, quality control of newly synthesized proteins and organelle communication. Constant ER turnover and modulation is needed to meet different cellular requirements and autophagy has an important role in this process. However, its underlying regulatory mechanisms remain unexplained. Here we show that members of the FAM134 reticulon protein family are ER-resident receptors that bind to autophagy modifiers LC3 and GABARAP, and facilitate ER degradation by autophagy ('ER-phagy'). Downregulation of FAM134B protein in human cells causes an expansion of the ER, while FAM134B overexpression results in ER fragmentation and lysosomal degradation. Mutant FAM134B proteins that cause sensory neuropathy in humans are unable to act as ER-phagy receptors. Consistently, disruption of Fam134b in mice causes expansion of the ER, inhibits ER turnover, sensitizes cells to stress-induced apoptotic cell death and leads to degeneration of sensory neurons. Therefore, selective ER-phagy via FAM134 proteins is indispensable for mammalian cell homeostasis and controls ER morphology and turnover in mice and humans.
journal_name
Naturejournal_title
Natureauthors
Khaminets A,Heinrich T,Mari M,Grumati P,Huebner AK,Akutsu M,Liebmann L,Stolz A,Nietzsche S,Koch N,Mauthe M,Katona I,Qualmann B,Weis J,Reggiori F,Kurth I,Hübner CA,Dikic Idoi
10.1038/nature14498subject
Has Abstractpub_date
2015-06-18 00:00:00pages
354-8issue
7556eissn
0028-0836issn
1476-4687pii
nature14498journal_volume
522pub_type
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