PI4P and BLOC-1 remodel endosomal membranes into tubules.
PI4P and BLOC-1 remodel endosomal membranes into tubules.
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DOI:
10.1083/jcb.202110132
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发表时间:
2022-11-07
影响因子:
7.8
通讯作者:
Delevoye, Cedric
中科院分区:
文献类型:
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作者:
Jani, Riddhi Atul;Di Cicco, Aurelie;Keren-Kaplan, Tal;Vale-Costa, Silvia;Hamaoui, Daniel;Hurbain, Ilse;Tsai, Feng-Ching;Di Marco, Mathilde;Mace, Anne-Sophie;Zhu, Yueyao;Amorim, Maria Joao;Bassereau, Patricia;Bonifacino, Juan S.;Subtil, Agathe;Marks, Michael S.;Levy, Daniel;Raposo, Graca;Delevoye, Cedric
Tubular recycling endosomes originate from early endosomes to deliver contents to target membranes. Jani et al. show that BLOC-1 and PI4P (synthesized by PI4KIIs) remodel membranes to generate and stabilize recycling tubules for cargo trafficking and exploitation by pathogens. Intracellular trafficking is mediated by transport carriers that originate by membrane remodeling from donor organelles. Tubular carriers contribute to the flux of membrane lipids and proteins to acceptor organelles, but how lipids and proteins impose a tubular geometry on the carriers is incompletely understood. Using imaging approaches on cells and in vitro membrane systems, we show that phosphatidylinositol-4-phosphate (PI4P) and biogenesis of lysosome-related organelles complex 1 (BLOC-1) govern the formation, stability, and functions of recycling endosomal tubules. In vitro, BLOC-1 binds and tubulates negatively charged membranes, including those containing PI4P. In cells, endosomal PI4P production by type II PI4-kinases is needed to form and stabilize BLOC-1-dependent recycling endosomal tubules. Decreased PI4KIIs expression impairs the recycling of endosomal cargoes and the life cycles of intracellular pathogens such as Chlamydia bacteria and influenza virus that exploit the membrane dynamics of recycling endosomes. This study demonstrates how a phospholipid and a protein complex coordinate the remodeling of cellular membranes into functional tubules.
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影响因子:
11.8
作者:
Chang-Ileto, Belle;Frere, Samuel G.;Chan, Robin B.;Voronov, Sergey V.;Roux, Aurelian;Di Paolo, Gilbert
通讯作者:
Di Paolo, Gilbert
影响因子:
5.4
作者:
Amorim, Maria Joao;Bruce, Emily A.;Digard, Paul
通讯作者:
Digard, Paul
影响因子:
3.4
作者:
Allgood SC;Neunuebel MR
通讯作者:
Neunuebel MR
影响因子:
64.5
作者:
Dippold HC;Ng MM;Farber-Katz SE;Lee SK;Kerr ML;Peterman MC;Sim R;Wiharto PA;Galbraith KA;Madhavarapu S;Fuchs GJ;Meerloo T;Farquhar MG;Zhou H;Field SJ
通讯作者:
Field SJ
影响因子:
21.3
作者:
通讯作者:
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