PUBLICATION

A Golgi-derived vesicle potentiates PtdIns4P to PtdIns3P conversion for endosome fission

Authors
Gong, B., Guo, Y., Ding, S., Liu, X., Meng, A., Li, D., Jia, S.
ID
ZDB-PUB-210922-1
Date
2021
Source
Nature cell biology   23: 782-795 (Journal)
Registered Authors
Gong, Bo, Jia, Shunji, Li, Dong, Meng, Anming
Keywords
none
MeSH Terms
  • Animals
  • COS Cells
  • Carrier Proteins/genetics
  • Carrier Proteins/metabolism*
  • Chlorocebus aethiops
  • Class III Phosphatidylinositol 3-Kinases/genetics
  • Class III Phosphatidylinositol 3-Kinases/metabolism
  • Endoplasmic Reticulum/genetics
  • Endoplasmic Reticulum/metabolism*
  • Endosomes/genetics
  • Endosomes/metabolism*
  • Golgi Apparatus/genetics
  • Golgi Apparatus/metabolism*
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Phosphatidylinositol Phosphates/metabolism*
  • Protein Transport
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
PubMed
34183801 Full text @ Nat. Cell Biol.
Abstract
Endosome fission is essential for cargo sorting and targeting in the endosomal system. However, whether organelles other than the endoplasmic reticulum (ER) participate in endosome fission through membrane contacts is unknown. Here, we characterize a Golgi-derived vesicle, the SEC14L2 compartment, that plays a unique role in facilitating endosome fission through ternary contacts with endosomes and the ER. Localized to the ER-mediated endosome fission site, the phosphatidylinositol transfer protein SEC14L2 promotes phosphatidylinositol 4-phosphate (PtdIns4P) to phosphatidylinositol 3-phosphate (PtdIns3P) conversion before endosome fission. In the absence of SEC14L2, endosome fission is attenuated and more enlarged endosomes arise due to endosomal accumulation of PtdIns4P and reduction in PtdIns3P. Collectively, our data suggest roles of the Golgi network in ER-associated endosome fission and a mechanism involving ER-endosome contacts in the regulation of endosomal phosphoinositide conversion.
Genes / Markers
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Human Disease / Model
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