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Comparative phenotypic analysis of the two major splice isoforms of phosphatidylinositol phosphate kinase type I gamma in vivo

MPS-Authors
http://pubman.mpdl.mpg.de/cone/persons/resource/persons78312

Legate,  Kyle R.
Fässler, Reinhard / Molecular Medicine, Max Planck Institute of Biochemistry, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons77774

Böttcher,  Ralph T.
Fässler, Reinhard / Molecular Medicine, Max Planck Institute of Biochemistry, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons78778

Takahashi,  Seiichiro
Fässler, Reinhard / Molecular Medicine, Max Planck Institute of Biochemistry, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons77945

Fässler,  Reinhard
Fässler, Reinhard / Molecular Medicine, Max Planck Institute of Biochemistry, Max Planck Society;

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Citation

Legate, K. R., Montag, D., Böttcher, R. T., Takahashi, S., & Fässler, R. (2012). Comparative phenotypic analysis of the two major splice isoforms of phosphatidylinositol phosphate kinase type I gamma in vivo. JOURNAL OF CELL SCIENCE, 125(23), 5636-5646. doi:10.1242/jcs.102145.


Cite as: http://hdl.handle.net/11858/00-001M-0000-000E-ED60-E
Abstract
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 I gamma (PIPKI gamma), encoded by the gene Pip5k1c, versus ablation of a specific splice isoform, PIPKI gamma_i2, with respect to three reported PIPKI gamma functions. Ablation of PIPKI gamma_i2 caused a neuron-specific endocytosis defect similar to that found in PIPKI gamma(-/-) mice, while agonist-induced calcium signaling was reduced in PIPKI gamma(-/-) cells, but was not affected in the absence of PIPKI gamma_i2. A reported contribution of PIPKI gamma to epithelial integrity was not evident in PIPKI gamma(-/-) mice. Given that mice lacking PIPKI gamma_i2 live a normal lifespan whereas PIPKI gamma(-/-) mice die shortly after birth, we propose that PIPKI gamma-mediated metabotropic calcium signaling may represent an essential function of PIPKI gamma, whereas functions specific to the PIPKI gamma_i2 splice isoform are not essential for survival.