Diacylglycerol Kinase δ Suppresses ER-to-Golgi Traffic via Its SAM and PH Domains

• Hisao Nagaya

  Department of Biochemistry, Sapporo Medical University School of Medicine, Sapporo 060-8556, Japan;

• Ikuo Wada

  Department of Biochemistry, Sapporo Medical University School of Medicine, Sapporo 060-8556, Japan;

• Yan-Jun Jia

  Department of Biochemistry, Sapporo Medical University School of Medicine, Sapporo 060-8556, Japan;

• Hideo Kanoh

  Department of Biochemistry, Sapporo Medical University School of Medicine, Sapporo 060-8556, Japan;

• Randy W. Schekman

  editor

抄録

We report here that the anterograde transport from the endoplasmic reticulum (ER) to the Golgi was markedly suppressed by diacylglycerol kinase δ (DGKδ) that uniquely possesses a pleckstrin homology (PH) and a sterile α motif (SAM) domain. A low-level expression of DGKδ in NIH3T3 cells caused redistribution into the ER of the marker proteins of the Golgi membranes and the vesicular-tubular clusters (VTCs). In this case DGKδ delayed the ER-to-Golgi traffic of vesicular stomatitis virus glycoprotein (VSV G) and also the reassembly of the Golgi apparatus after brefeldin A (BFA) treatment and washout. DGKδ was demonstrated to associate with the ER through its C-terminal SAM domain acting as an ER-targeting motif. Both of the SAM domain and the N-terminal PH domain of DGKδ were needed to exert its effects on ER-to-Golgi traffic. Kinase-dead mutants of DGKδ were also effective as the wild-type enzyme, suggesting that the catalytic activity of DGK was not involved in the present observation. Remarkably, the expression of DGKδ abrogated formation of COPII-coated structures labeled with Sec13p without affecting COPI structures. These findings indicate that DGKδ negatively regulates ER-to-Golgi traffic by selectively inhibiting the formation of ER export sites without significantly affecting retrograde transport.

収録刊行物

• Molecular Biology of the Cell

  Molecular Biology of the Cell 13 (1), 302-316, 2002-01

  American Society for Cell Biology (ASCB)

キーワード

• Cell Biology
• Molecular Biology

詳細情報

• CRID: 1364233270444984576
• NII論文ID: 30018378063
• DOI: 10.1091/mbc.01-05-0255
• ISSN: 19394586
• ISSN: 10591524
• ISSN: http://id.crossref.org/issn/10591524
• データソース種別:
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  • CiNii Articles