Article abstract
Nature Cell Biology 10, 1135 - 1145 (2008)
Published online: 14 September 2008 | doi:10.1038/ncb1773
GPHR is a novel anion channel critical for acidification and functions of the Golgi apparatus
Yusuke Maeda1,2,3, Toru Ide4,5, Masato Koike6,8, Yasuo Uchiyama6,8 & Taroh Kinoshita1,2,7
Abstract
The organelles within secretory and endocytotic pathways in mammalian cells have acidified lumens, and regulation of their acidic pH is critical for the trafficking, processing and glycosylation of cargo proteins and lipids, as well as the morphological integrity of the organelles. How organelle lumen acidification is regulated, and how luminal pH elevation disturbs these fundamental cellular processes, is largely unknown. Here, we describe a novel molecule involved in Golgi acidification. First, mutant cells defective in Golgi acidification were established that exhibited delayed protein transport, impaired glycosylation and Golgi disorganization. Using expression cloning, a novel Golgi-resident multi-transmembrane protein, named Golgi pH regulator (GPHR), was identified as being responsible for the mutant cells. After reconstitution in planar lipid bilayers, GPHR exhibited a voltage-dependent anion-channel activity that may function in counterion conductance. Thus, GPHR modulates Golgi functions through regulation of acidification.
- Research Institute for Microbial Diseases, Osaka University, Suita, Osaka 565–0871, Japan.
- WPI Immunology Frontier Research Center, Osaka University, Suita, Osaka 565–0871, Japan.
- PRESTO Japan Science and Technology Agency, Saitama 332–0012, Japan.
- Laboratories for Nanobiology, Graduate School of Frontier Biosciences, Osaka University, Suita, Osaka 565–0871, Japan.
- Molecular-Informational Life Science Research Group, RIKEN, Wako 351–0198, Japan.
- Department of Cell Biology and Neurosciences, Graduate School of Medicine, Osaka University, Suita, Osaka 565–0871, Japan.
- CREST, Japan Science and Technology Agency, Saitama 332–0012, Japan.
- Current address: Department of Cell Biology and Neuroscience, Juntendo University School of Medicine, Tokyo 113–8421, Japan.
Correspondence to: Yusuke Maeda1,2,3 e-mail: ymaeda@biken.osaka-u.ac.jp
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