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Phosphatidylinositol phosphate kinase type 1γ (PIPKIγ) is a key enzyme in the generation of phosphatidylinositol 4,5-bisphosphate [PI(4,5)P(2)] and is expressed at high levels in the nervous system. Homozygous knockout mice lacking this enzyme die postnatally within 24 h, whereas PIPKIγ(+/-) siblings breed normally and have no reported phenotype. Here we show that adult PIPKIγ(+/-) mice have dramatically elevated hearing thresholds for high-frequency sounds. During the first postnatal week we observed a reduction of ATP-dependent Ca(2+) signaling activity in cochlear nonsensory cells. Because Ca(2+) signaling under these conditions depends on inositol-1,4,5-trisphosphate generation from phospholipase C (PLC)-dependent hydrolysis of PI(4,5)P(2), we conclude that (i) PIPKIγ is primarily responsible for the synthesis of the receptor-regulated PLC-sensitive PI(4,5)P(2) pool in the cell syncytia that supports auditory hair cells; (ii) spatially graded impairment of this signaling pathway in cochlear nonsensory cells causes a selective alteration in the acquisition of hearing in PIPKIγ(+/-) mice. This mouse model also suggests that PIPKIγ may determine the level of gap junction contribution to cochlear development.

Reduced phosphatidylinositol 4,5-bisphosphate synthesis impairs inner ear Ca 2+ signaling and high-frequency hearing acquisition

Reduced phosphatidylinositol 4,5-bisphosphate synthesis impairs inner ear Ca ²⁺ signaling and high-frequency hearing acquisition