https://scholars.lib.ntu.edu.tw/handle/123456789/416734
標題: | Action of Arl1 GTPase and golgin Imh1 in Ypt6-independent retrograde transport from endosomes to the trans-Golgi network | 作者: | Chen, Yan-Ting Wang, I-Hao Wang, Yi-Hsun Chiu, Wan-Yun Hu, Jen-Hao Chen, Wen-Hui Fang-Jen Scott Lee |
公開日期: | 2019 | 出版社: | AMER SOC CELL BIOLOGY | 卷: | 30 | 期: | 8 | 起(迄)頁: | 1008 | 來源出版物: | Molecular biology of the cell | 摘要: | The Arf and Rab/Ypt GTPases coordinately regulate membrane traffic and organelle structure by regulating vesicle formation and fusion. Ample evidence has indicated that proteins in these two families may function in parallel or complementarily; however, the manner in which Arf and Rab/Ypt proteins perform interchangeable functions remains unclear. In this study, we report that a Golgi-localized Arf, Arl1, could suppress Ypt6 dysfunction via its effector golgin, Imh1, but not via the lipid flippase Drs2. Ypt6 is critical for the retrograde transport of vesicles from endosomes to the trans-Golgi network (TGN), and its mutation leads to severe protein mislocalization and growth defects. We first overexpress the components of the Arl3-Syt1-Arl1-Imh1 cascade and show that only Arl1 and Imh1 can restore endosome-to-TGN trafficking in ypt6-deleted cells. Interestingly, increased abundance of Arl1 or Imh1 restores localization of the tethering factor Golgi associated retrograde-protein (GARP) complex to the TGN in the absence of Ypt6. We further show that the N-terminal domain of Imh1 is critical for restoring GARP localization and endosome-to-TGN transport in ypt6-deleted cells. Together, our results reveal the mechanism by which Arl1-Imh1 facilitates the recruitment of GARP to the TGN and compensates for the endosome-to-TGN trafficking defects in dysfunctional Ypt6 conditions. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-85064000999&doi=10.1091%2fmbc.E18-09-0579&partnerID=40&md5=dde3535fce79d7b998761d6628bf4f20 https://scholars.lib.ntu.edu.tw/handle/123456789/416734 |
ISSN: | 1059-1524 | DOI: | 10.1091/mbc.E18-09-0579 |
顯示於: | 分子醫學研究所 |
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