| First Author | Yamazaki M | Year | 2013 |
| Journal | Neurosci Lett | Volume | 547 |
| Pages | 59-64 | PubMed ID | 23680464 |
| Mgi Jnum | J:201109 | Mgi Id | MGI:5510939 |
| Doi | 10.1016/j.neulet.2013.04.062 | Citation | Yamazaki M, et al. (2013) Phosphatidylinositol 4-phosphate 5-kinase beta regulates growth cone morphology and semaphorin 3A-triggered growth cone collapse in mouse dorsal root ganglion neurons. Neurosci Lett 547:59-64 |
| abstractText | Growth cone motility and morphology, which are critical for axon guidance, are controlled through intracellular events such as actin cytoskeletal reorganization and vesicular trafficking. The membrane phospholipid phosphatidylinositol 4,5-bisphosphate [PI(4,5)P(2)] has been implicated in regulation of these cellular processes in a diverse range of cell types. The main kinases involved in the production of PI(4,5)P(2) are the type I phosphatidylinositol 4-phosphate 5-kinase (PIP5K) family, which consist of three isozymes, alpha, beta and gamma. Here, we demonstrate the involvement of PIP5Kbeta in growth cone dynamics. Overexpression of a lipid kinase-deficient mutant of PIP5Kbeta (PIP5Kbeta-KD) in mouse dorsal root ganglion (DRG) neurons stimulated axon elongation and increased growth cone size, whereas wild-type PIP5Kbeta tended to show opposite effects. Furthermore, PIP5Kbeta-KD inhibited growth cone collapse of DRG neurons induced by semaphorin 3A (Sema3A). These results provide evidence that PIP5Kbeta negatively regulates axon elongation and growth cone size and is involved in the cellular signaling pathway for Sema3A-triggered repulsion in DRG neurons. |
