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. 2021 Sep 9;12:5354. doi: 10.1038/s41467-021-25621-4

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© The Author(s) 2021

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. 8 — Mitochondrial division initiates at contacts with the ER, where the ER drives the constriction of mitochondrial membranes. This implicates an actin machinery that involves the ER protein INF2 and the mitochondrial Spire1C. The constriction allows the recruitment of Drp1 by adapters such as MFF and its oligomerization that further constrict mitochondrial membranes (non-represented in the cartoon). Lysosomes are then recruited to the division site in a process mediated by the Rab7-ORP1L-VAPs interaction that establishs contact sites with the ER (1). This allows the formation of a three-way contact between the ER, the lysosome and mitochondria at the division site that brings the lysosome in contact with mitochondria. Lysosome-mitochondria tethers are still unknown. At the Lysosome-mitochondria contact (2), we propose that ORP1L mediates the transfer of PI(4)P from lysosome to the division site. This model is supported by the impaired mitochondrial division when this transfer is inhibited or when PI(4)P is depleted at the mitochondrial division site.