4.7 Article

PI4P and BLOC-1 remodel endosomal membranes into tubules

期刊

JOURNAL OF CELL BIOLOGY
卷 221, 期 11, 页码 -

出版社

ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.202110132

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资金

  1. National Institutes of Health [R01 EY015625]
  2. GENESPOIR
  3. Institut National de la Sante et de la Recherche Medicale (INSERM)
  4. Institut Curie
  5. Centre National de la Recherche Scientifique (CNRS)
  6. Institut Pasteur
  7. Intramural Program of NICHD, NIH [ZIA-HD001607]
  8. LabEx CellTisPhyBio [ANR-10-LABX-0038, ANR-11-LABX-0038, ANR-10-IDEX-0001-02]
  9. French National Research Infrastructure France-BioImaging [ANR10-INBS-04]
  10. European Research Council under the European Union [101001521]
  11. Portuguese Fundacao para a Ciencia e a Tecnologia [CEECIND/02373/2020]
  12. Fundacao para a Ciencia e a Tecnologia (FCT)
  13. Instituto Gulbenkian de Ciencia (IGC, Portugal)
  14. Ligue contre le Cancer
  15. European Research Council (ERC) [101001521] Funding Source: European Research Council (ERC)

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Intracellular trafficking is mediated by transport carriers that originate by membrane remodeling from donor organelles. Phosphatidylinositol-4-phosphate (PI4P) and biogenesis of lysosome-related organelles complex 1 (BLOC-1) play important roles in the formation, stability, and functions of recycling endosomal tubules.
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 PI4kinases 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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