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. 2020 Nov 3;11:5559. doi: 10.1038/s41467-020-19032-0

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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. 10 — Model for MCC and Rab7 function in lysosomal cholesterol export. The trimeric Mon1-Ccz1-C18orf8 (MCC) GEF activates mammalian Rab7, which binds the NPC1 cholesterol transporter and either a) directly activates NPC1’s cholesterol export function; or b) assembles a down-stream membrane contact site (MCS) at which a yet-uncharacterised lipid transfer protein (LTP) mediates cholesterol transfer to the ER and/or plasma membrane. A combined Rab7 function in NPC1 activation and MCS formation would assure lysosomal cholesterol export only proceeds once a down-stream lipid transfer module is assembled.

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