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Sphingolipid metabolic flow controls phosphoinositide turnover at the trans ‐Golgi network
Author(s) -
Capasso Serena,
Sticco Lucia,
Rizzo Riccardo,
Pirozzi Marinella,
Russo Domenico,
Dathan Nina A,
Campelo Felix,
Galen Josse,
HölttäVuori Maarit,
Turacchio Gabriele,
Hausser Angelika,
Malhotra Vivek,
Riezman Isabelle,
Riezman Howard,
Ikonen Elina,
Luberto Chiara,
Parashuraman Seetharaman,
Luini Alberto,
D'Angelo Giovanni
Publication year - 2017
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.15252/embj.201696048
Subject(s) - library science , research council , national library , biology , political science , computer science , linguistics , philosophy , government (linguistics)
Sphingolipids are membrane lipids globally required for eukaryotic life. The sphingolipid content varies among endomembranes with pre‐ and post‐Golgi compartments being poor and rich in sphingolipids, respectively. Due to this different sphingolipid content, pre‐ and post‐Golgi membranes serve different cellular functions. The basis for maintaining distinct subcellular sphingolipid levels in the presence of membrane trafficking and metabolic fluxes is only partially understood. Here, we describe a homeostatic regulatory circuit that controls sphingolipid levels at the trans ‐Golgi network ( TGN ). Specifically, we show that sphingomyelin production at the TGN triggers a signalling pathway leading to PtdIns(4) P dephosphorylation. Since PtdIns(4) P is required for cholesterol and sphingolipid transport to the trans ‐Golgi network, PtdIns(4) P consumption interrupts this transport in response to excessive sphingomyelin production. Based on this evidence, we envisage a model where this homeostatic circuit maintains a constant lipid composition in the trans ‐Golgi network and post‐Golgi compartments, thus counteracting fluctuations in the sphingolipid biosynthetic flow.