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Published 20 December 2004. doi:10.1083/jcb.200408008
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 167, Number 6, 1005-1010
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 Critical role of PIP5KI{gamma}87 in InsP3-mediated Ca2+ signaling

Ying Jie Wang1, Wen Hong Li2, Jing Wang1, Ke Xu2, Ping Dong1, Xiang Luo1, and Helen L. Yin1

1 Department of Physiology and 2 Department of Cell Biology, University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390

Correspondence to Helen L. Yin: Helen.Yin{at}UTSouthwestern.edu


Abstract
Phosphatidylinositol 4,5-bisphosphate (PIP2) is the obligatory precursor of inositol 1,4,5-trisphosphate (InsP3 or IP3) and is therefore critical to intracellular Ca2+ signaling. Using RNA interference (RNAi), we identified the short splice variant of type I phosphatidylinositol 4-phosphate 5-kinase {gamma} (PIP5KI{gamma}87) as the major contributor of the PIP2 pool that supports G protein–coupled receptor (GPCR)-mediated IP3 generation. PIP5KI{gamma}87 RNAi decreases the histamine-induced IP3 response and Ca2+ flux by 70%. Strikingly, RNAi of other PIP5KI isoforms has minimal effect, even though some of these isoforms account for a larger percent of total PIP2 mass and have previously been implicated in receptor mediated endocytosis or focal adhesion formation. Therefore, PIP5KI{gamma}87's PIP2 pool that supports GPCR-mediated Ca2+ signaling is functionally compartmentalized from those generated by the other PIP5KIs.

Abbreviations used in this paper: [Ca2+]i, intracellular Ca2+ concentration; GPCR, G protein–coupled receptor; IP3, inositol 1,4,5-trisphosphate; PIP5KI{gamma}, type I phosphatidylinositol 4-phosphate 5-kinase {gamma}; PIP2, phosphatidylinositol 4,5-bisphosphate; PM, plasma membrane; RNAi, RNA interference; siRNA, small interfering RNA.


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