Oral Presentation 2019 Hunter Cell Biology Meeting

ORP1L regulates cholesterol exit from late endosomes and lysosomes: a role for phosphatidylinositol biphosphates (#65)

Hongyuan Robert Yang 1 , Andrew J Brown 1 , Jia-Wei Wu 2 3
  1. School of Biotechnology and Biomolecular Sciences, The University of New South Wales, Sydney, NSW, Australia
  2. Beijing Advanced Innovation Center for Structural Biology, MOE Key Laboratory for Protein Science, Tsinghua-Peking Center for Life Sciences, School of Life Sciences, Tsinghua University, Beijing, China
  3. Institute of Molecular Enzymology, Soochow University, Suzhou, Jiangsu, China

Phosphatidylinositol phosphates (PIPs) and cholesterol are known to regulate the function of late endosomes and lysosomes (LELs). ORP1L, a putative lipid sensor/transporter, specifically localizes to LELs. Here, we show that the highly conserved lipid-binding domain of ORP1, ORP1-ORD, can transport sterols between membranes only in the presence of PI(4,5)P2 or PI(3,4)P2. Surprisingly however, ORP1-ORD can’t transport any PIPs in vitro. In cells, both ORP1L and PI(3,4)P2 were required for the efficient removal of cholesterol from LELs. The crystal structures of ORP1-ORD in complex with cholesterol or PI(4,5)P2 reveal that the N-terminal loop and the lid of ORP1-ORD play important roles in ORD oligomerization and function, and that the 5- or 3-phosphate group of PI(4,5)P2 or PI(3,4)P2 may facilitate ORP1-mediated cholesterol transport by keeping the lid of ORP1-ORD open. We further demonstrate that ORP1L can regulate mTORC1 signaling and autophagosome maturation by maintaining lysosomal lipid homeostasis. Thus, our work unveils a novel mechanism by which PIPs may regulate OSBP/ORPs-mediated transport of major lipid species such as cholesterol.    

Hongyuan Yang, Email: h.rob.yang@unsw.edu.au