Abstract
A number of membrane trafficking components are associated with lipid droplets (LDs) and/or are involved in their biogenesis. In this issue of The EMBO Journal, Li et al () show that the mammalian TRAPPII (TRAnsport Protein Particle) complex acts as an LD‐associated GEF for Rab18, thereby regulating LD homeostasis.
Highlights
A number of membrane trafficking components are associated with lipid droplets (LDs) and/or are involved in their biogenesis
Despite the fact that almost 40 different Rab GTPases have been found to associate with LDs, functional data regarding their role in LD biogenesis are available for only a few of them (Rab1, Rab5, Rab7, Rab8a, Rab32, Rab40c, and Rab18)
The most convincing evidence supporting a role for Rab18 in LD homeostasis comes from the observation of an accumulation of enlarged lipid droplets in fibroblasts from patients affected by Warburg Micro syndrome, a neurological syndrome caused by mutations in Rab18, in Rab3GAP1/Rab3GAP2, which works as a guanine nucleotide exchange factors (GEFs) for Rab18, or in TBC1D20, a Rab18 GTPase-activating protein (GAP) (Handley et al, 2015)
Summary
A number of membrane trafficking components are associated with lipid droplets (LDs) and/or are involved in their biogenesis. By adopting a combination of siRNA and gene-editing experiments, they demonstrate that the mammalian TRAPP (TRAnsport Protein Particle) complex, and in particular TRAPPII, acts as a LD-associated GEF for Rab18. Several TRAPP complexes have been isolated in yeast (TRAPPI, TRAPPII, TRAPPIII, and, very recently, TRAPPIV) (Kim et al, 2016; Lipatova et al, 2016) sharing the same core subunits but containing distinct peripheral subunits.
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