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Golgin‐97 facilitates Golgi Export of Inward Rectifier Potassium Channel
Author(s) -
TANEJA TARVINDER KAUR,
Ma Donghui,
Welling Paul A
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.860.7
Subject(s) - golgi apparatus , microbiology and biotechnology , cytoplasm , potassium channel , chemistry , inward rectifier potassium ion channel , mutant , biophysics , biology , biochemistry , ion channel , receptor , endoplasmic reticulum , gene
The inward rectifying potassium channel, Kir2.1, is selected as cargo into trans‐Golgi export carriers through a unique signal‐dependent mechanism. Mutations in the signal or depletion of the trafficking machinery (AP‐1) that decodes it prevents export of the channel from the TGN. Surprisingly, they also cause marked accumulation of the channel throughout the entire Golgi apparatus, suggesting anterograde transport of Kir2.1 through the Golgi may be closely coupled to its export from the TGN. Here we explore the mechanism. A systematic screen of Golgi tethers indentified Golgin‐97 as a Kir2.1 binding partner. In vitro studies revealed the interaction is direct, occurring between the GRIP domain of Golgin‐97 and the cytoplasmic domain of Kir2.1. Imaging and interaction studies in cells revealed that Golgi‐97 binds to the channel en route through the Golgi. Knockdown of Golgin‐97 using siRNA prevented exit of Kir2.1 from the Golgi. These observations are consistent with the idea that Golgin‐97 directly interacts with Kir2.1 in the cis‐Golgi for selection into specialized exit sites of the TGN. This project was supported by funds from NIH and American Heart Association.