NDLI: Regulation of NGF-driven neurite outgrowth by $Ins(1,4,5)P_{3}$ kinase is specifically associated with the two isoenzymes Itpka and Itpkb in a model of PC12 cells

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Regulation of NGF-driven neurite outgrowth by $Ins(1,4,5)P_{3}$ kinase is specifically associated with the two isoenzymes Itpka and Itpkb in a model of PC12 cells

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Koenig, Sandra Moreau, Colette Dupont, Geneviève Scoumanne, Ariane Erneux, Christophe
Description	Country affiliation: Belgium Author Affiliation: Koenig S ( Interdisciplinary Research Institute, Université Libre de Bruxelles, Brussels, Belgium.); Moreau C ( Interdisciplinary Research Institute, Université Libre de Bruxelles, Brussels, Belgium.); Dupont G ( Unité de Chronobiologie Théorique, Faculté des Sciences, Université Libre de Bruxelles, Brussels, Belgium.); Scoumanne A ( Laboratory of Functional Genetics, GIGA Signal Transduction, Université de Liège, Liège, Belgium.); Erneux C ( Interdisciplinary Research Institute, Université Libre de Bruxelles, Brussels, Belgium.)
Abstract	Four inositol phosphate kinases catalyze phosphorylation of the second messenger inositol 1,4,5-trisphosphate $[Ins(1,4,5)P_{3}]$ to inositol 1,3,4,5-tetrakisphosphate $[Ins(1,3,4,5)P_{4}]:$ these enzymes comprise three isoenzymes of inositol 1,4,5-trisphosphate 3-kinase (Itpk), referred to as Itpka, Itpkb and Itpkc, and the inositol polyphosphate multikinase (IPMK). The four enzymes that act on $Ins(1,4,5)P_{3}$ are all expressed in rat pheochromocytoma PC12 cells, a model that is used to study neurite outgrowth induced by nerve growth factor (NGF). We compared the effect of over-expression of the four GFP-tagged kinases on NGF-induced neurite outgrowth. Our data show that over-expression of the Itpka and Itpkb isoforms inhibits NGF-induced neurite outgrowth, but over-expression of Itpkc and IPMK does not. Surprisingly, over-expression of the N-terminal F-actin binding domain of Itpka, which lacks catalytic activity, was as effective at inhibiting neurite outgrowth as the full-length enzyme. Neurite length was also significantly decreased in cells over-expressing Itpka and Itpkb but not Itpkc or IPMK. This result did not depend on the over-expression level of any of the kinases. PC12 cells over-expressing GFP-tagged kinase-dead mutants Itpka/b have shorter neurites than GFP control cells. The decrease in neurite length was never as pronounced as observed with wild-type GFP-tagged Itpka/b. Finally, the percentage of neurite-bearing cells was increased in cells over-expressing the membranous type I $Ins(1,4,5)P_{3}$ 5-phosphatase. We conclude that Itpka and Itpkb inhibit neurite outgrowth through both F-actin binding and localized $Ins(1,4,5)P_{3}$ 3-kinase activity. Itpkc and IPMK do not influence neurite outgrowth or neurite length in this model.
File Format	HTM / HTML
ISSN	1742464X
Issue Number	13
Volume Number	282
e-ISSN	17424658
Journal	FEBS Journal
Language	English
Publisher	Wiley (on behalf of the Federation of European Biochemical Societies)
Publisher Date	2015-07-01
Publisher Place	Great Britain (UK)
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Biochemistry Isoenzymes Physiology Nerve Growth Factor Pharmacology Neurites Phosphotransferases (alcohol Group Acceptor) Actins Chemistry Animals Green Fluorescent Proteins Metabolism Pc12 Cells Rats Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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Regulation of NGF-driven neurite outgrowth by $Ins(1,4,5)P_{3}$ kinase is specifically associated with the two isoenzymes Itpka and Itpkb in a model of PC12 cells