GPHR is a novel anion channel critical for acidification and functions of the Golgi apparatus

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 lum...

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Published inNature cell biology Vol. 10; no. 10; pp. 1135 - 1145
Main Authors Ide, Toru, Maeda, Yusuke, Kinoshita, Taroh, Uchiyama, Yasuo, Koike, Masato
Format Journal Article
LanguageEnglish
Published England Nature Publishing Group 01.10.2008
Subjects
Acid deposition
Acidification
Amino Acid Sequence
Animals
Biology
CHO Cells
Cloning
Cricetinae
Cricetulus
Genetic aspects
Glycosylation
Golgi apparatus
Golgi Apparatus - enzymology
Golgi Apparatus - metabolism
Golgi Apparatus - ultrastructure
Humans
Ion channels
Ion Channels - chemistry
Ion Channels - metabolism
Lipids
Mammals
Molecular Sequence Data
Morphology
Mutants
Mutation - genetics
Phenotype
Physiological aspects
Protein Biosynthesis
Protein Structure, Quaternary
Protein Transport
Proteins
Protons
Vacuolar Proton-Translocating ATPases - metabolism
Japan
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Summary: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.
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ISSN:1465-7392
1476-4679
DOI:10.1038/ncb1773