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. 2020 Nov 16;11(11):983. doi: 10.1038/s41419-020-03195-1

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — In the meantime, LIR binds to the autophagosome generating a pulling force, so that the ER membrane forms vesicles, which pinch off and are then engulfed by the phagophore. CAMK2B phosphorylates FAM134B leading to oligomerization, ER fragmentation, and ER-phagy. High levels of AMFR lead to destabilized OMM and exposed IMM. FAM134B promotes the formation of the mitophagophore by interacting with OPA1. Besides, by potentiating mitophagy, it improves preadipocytes differentiation. CANX recognizes misfolded procollagens and interacts with FAM134B. Next, FAM134B binds to the autophagosome and delivers cargos to the lysosome for degradation. ATZ polymers are degraded through the ERLAD pathway. In this process, FAM134B helps the polymers enter the vesicles from the ER domain, and promotes the docking of these ER-derived vesicles to lysosomes. CANX segregates ATZ polymers into ER subdomains and forms a CNX:FAM134B:LC3B complex for the next step. In the liver, starvation induces C/EBPβ expression, which then increases the expression of FAM134B-2. FAM134B-2 interacts with LC3B and its lysosomal degradation is increased under starvation, indicating that it plays a role in starvation-induced hepatic ER-phagy.