| First Author | Legate KR | Year | 2012 |
| Journal | J Cell Sci | Volume | 125 |
| Issue | Pt 23 | Pages | 5636-46 |
| PubMed ID | 22976293 | Mgi Jnum | J:200273 |
| Mgi Id | MGI:5507953 | Doi | 10.1242/jcs.102145 |
| Citation | Legate KR, et al. (2012) Comparative phenotypic analysis of the two major splice isoforms of phosphatidylinositol phosphate kinase type Igamma in vivo. J Cell Sci 125(Pt 23):5636-46 |
| abstractText | Localized production of polyphosphoinositides is critical for their signaling function. To examine the biological relevance of specific pools of phosphatidylinositol 4,5-bisphosphate we compared the consequences of genetically ablating all isoforms of phosphatidylinositol phosphate (PIP) kinase type Igamma (PIPKIgamma), encoded by the gene Pip5k1c, versus ablation of a specific splice isoform, PIPKIgamma_i2, with respect to three reported PIPKIgamma functions. Ablation of PIPKIgamma_i2 caused a neuron-specific endocytosis defect similar to that found in PIPKIgamma(-/-) mice, while agonist-induced calcium signaling was reduced in PIPKIgamma(-/-) cells, but was not affected in the absence of PIPKIgamma_i2. A reported contribution of PIPKIgamma to epithelial integrity was not evident in PIPKIgamma(-/-) mice. Given that mice lacking PIPKIgamma_i2 live a normal lifespan whereas PIPKIgamma(-/-) mice die shortly after birth, we propose that PIPKIgamma-mediated metabotropic calcium signaling may represent an essential function of PIPKIgamma, whereas functions specific to the PIPKIgamma_i2 splice isoform are not essential for survival. |
