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. 2022 Nov 3;30(3):753–765. doi: 10.1038/s41418-022-01080-2

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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. 9 — The ubiquitin ligase MARCH5 controls the stability of MCL1 during interphase. Mitotic degradation of MCL1 is proteasome-dependent but only partially dependent on MARCH5. Accordingly, MCL1 expression is elevated during early mitosis and takes longer to be depleted during mitotic arrest in MARCH5-depleted cells. NOXA is also stabilized in MARCH5-depleted cells in an MCL1-dependent manner. During late mitotic arrest, the destruction of MCL1 (by yet unidentified ubiquitin ligases X) and NOXA facilitates the activation of BAK and BAX. Our data suggest that the increase of mitochondrial DRP1 also plays a critical role in promoting mitotic apoptosis in the absence of MARCH5.