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Publication

VPS13B is localized at the cis-trans Golgi complex interface and is a functional partner of FAM177A1.

bioRxiv : the preprint server for biology | 2023

Mutations in VPS13B, a member of a protein family implicated in bulk lipid transport between adjacent membranes, cause Cohen syndrome. VPS13B is known to be concentrated in the Golgi complex, but its precise location within this organelle and thus the site(s) where it achieves lipid transport remains unclear. Here we show that VPS13B is localized at the interface between cis and trans Golgi sub-compartments and that Golgi complex re-formation after Brefeldin A (BFA) induced disruption is delayed in VPS13B KO cells. This delay is phenocopied by loss of FAM177A1, a Golgi complex protein of unknown function reported to be a VPS13B interactor and whose mutations also result in a developmental disorder. In zebrafish, the vps13b orthologue, not previously annotated in this organism, genetically interacts with fam177a1. Collectively, these findings raise the possibility that bulk lipid transport by VPS13B may play a role in expanding Golgi membranes and that VPS13B may be assisted in this function by FAM177A1.

Pubmed ID: 38187698 RIS Download

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Associated grants

Agency: NIGMS NIH HHS, United States
Id: R01 GM151829
Agency: NICHD NIH HHS, United States
Id: R01 HD110556
Agency: NINDS NIH HHS, United States
Id: R01 NS036251
Agency: NIH HHS, United States
Id: R01 OD011116

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