タナベ ケンジ
  田邊 賢司
   所属   研究施設 研究施設
   職種   准教授
論文種別 原著
言語種別 英語
査読の有無 査読あり
表題 PtdIns4KIIα generates endosomal PtdIns(4)P and is required for receptor sorting at early endosomes.
掲載誌名 正式名:Molecular biology of the cell
略  称:Mol Biol Cell
ISSNコード:(1939-4586)1059-1524(Linking)
掲載区分国外
巻・号・頁 27(6),pp.990-1001
著者・共著者 Henmi Yuji, Morikawa Yoshiaki, Oe Natsuko, Ikeda Narumi, Fujita Akikazu, Takei Kohji, Minogue Shane, Tanabe Kenji
担当区分 最終著者,責任著者
発行年月 2016/03
概要 Phosphatidylinositol 4-kinase IIα (PtdIns4KIIα) localizes to the trans-Golgi network and endosomal compartments and has been implicated in the regulation of endosomal traffic, but the role of both its enzymatic activity and the site of its action have not been elucidated. This study shows that PtdIns4KIIα is required for production of endosomal phosphatidylinositol 4-phosphate (PtdIns(4)P) on early endosomes and for the sorting of transferrin and epidermal growth factor receptor into recycling and degradative pathways. Depletion of PtdIns4KIIα with siRNA significantly reduced the amount of vesicular PtdIns(4)P on early endosomes but not on Golgi membranes. Cells depleted of PtdIns4KIIα had an impaired ability to sort molecules destined for recycling from early endosomes. We further identify the Eps15 homology domain-containing protein EHD3 as a possible endosomal effector of PtdIns4KIIα. Tubular endosomes containing EHD3 were shortened and became more vesicular in PtdIns4KIIα-depleted cells. Endosomal PtdIns(4,5)P2 was also significantly reduced in PtdIns4KIIα-depleted cells. These results show that PtdIns4KIIα regulates receptor sorting at early endosomes through a PtdIns(4)P-dependent pathway and contributes substrate for the synthesis of endosomal PtdIns(4,5)P2.
DOI 10.1091/mbc.E15-08-0564
PMID 26823017