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. 2021 Jan 20;10:5. doi: 10.1186/s40035-020-00229-8

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© The Author(s) 2021

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 6 — Model of disintegration of the ER–mitochondrial contact sites upon mitochondrial depolarization. Under basal conditions, the contacts between the ER and mitochondria are mediated by various proteins, including Mfn2, ubiquitination of which at K416 was suggested to promote the interaction (left panel). Upon mitochondrial depolarization, Mfn2 is polyubiquitinated and is removed from the membrane for proteasomal degradation, resulting in disruption of the ER–mitochondria contact sites and drifting of these organelles away from each other (right panel)