Impaired retrograde membrane traffic through endosomes in a mutant CHO cell defective in phosphatidylserine synthesis

Shoken Lee, Yasunori Uchida, Kazuo Emoto, Masato Umeda, Osamu Kuge, Tomohiko Taguchi, Hiroyuki Arai

研究成果: ジャーナルへの寄稿学術誌査読

31 被引用数 (Scopus)

抄録

Phosphatidylserine (PS), a relatively minor constituent in the plasma membrane (PM), participates in various cellular processes such as clearance of apoptotic cells and recruitment of signaling molecules. PS also localizes in the membranes of endocytic organelles, such as recycling endosomes (REs). We recently showed that in REs, PS binds to the pleckstrin homology (PH) domain of evectin-2, thereby regulating retrograde traffic from REs to the Golgi. However, direct evidence that PS has a role in retrograde traffic is lacking. Here, we examined the contribution of PS to endosomal membrane traffic by exploiting a mutant CHO cell line (PSA-3) that is defective in PS synthesis. In PSA-3 cells, the Golgi localization of TGN38, a protein that circulates between the Golgi and the PM through endosomes by retrograde traffic, was abolished, whereas the localizations of other organelle markers remained unchanged. Increasing the cellular PS level by adding ethanolamine to the culture medium restored the Golgi localization of TGN38. Tracking the endocytic fate of cell surface TGN38 that was labeled by anti-TGN38 antibody showed that retrograde transport of TGN38 was impaired at endosomes, not at the PM. These findings provide direct evidence that intracellular PS is required for retrograde traffic through endosomes.

本文言語英語
ページ(範囲)728-736
ページ数9
ジャーナルGenes to Cells
17
8
DOI
出版ステータス出版済み - 8月 2012

!!!All Science Journal Classification (ASJC) codes

  • 遺伝学
  • 細胞生物学

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