2024-03-29T10:38:21Z
https://tsukuba.repo.nii.ac.jp/oai
oai:tsukuba.repo.nii.ac.jp:00029278
2022-04-27T08:57:28Z
29:1294
3:62:5596:649
Phosphatidylinositol 4-phosphate 5-kinase β regulates growth cone morphology and Semaphorin 3A-triggered growth cone collapse in mouse dorsal root ganglion neurons
金保, 安則
Yamazaki, Masakazu
Yamauchi, Yohei
Goshima, Yoshio
Kanaho, Yasunori
© 2013 Elsevier Ireland Ltd.
NOTICE: this is the author's version of a work that was accepted for publication in Neuroscience letters. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Neuroscience letters, Vol.547, 28 June 2013,
http://dx.doi.org/10.1016/j.neulet.2013.04.062.
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)P2] 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)P2 are the type I phosphatidylinositol 4-phosphate 5-kinase (PIP5K) family, which consist of three isozymes, α, β and γ. Here, we demonstrate the involvement of PIP5Kβ in growth cone dynamics. Overexpression of a lipid kinase-deficient mutant of PIP5Kβ (PIP5Kβ-KD) in mouse dorsal root ganglion (DRG) neurons stimulated axon elongation and increased growth cone size, whereas wild-type PIP5Kβ tended to show opposite effects. Furthermore, PIP5Kβ-KD inhibited growth cone collapse of DRG neurons induced by semaphorin 3A (Sema3A). These results provide evidence that PIP5Kβ negatively regulates axon elongation and growth cone size and is involved in the cellular signaling pathway for Sema3A-triggered repulsion in DRG neurons.
Elsevier Ireland Ltd.
2013-06
eng
journal article
http://hdl.handle.net/2241/119594
https://tsukuba.repo.nii.ac.jp/records/29278
23680464
10.1016/j.neulet.2013.04.062
0304-3940
AA00754925
Neuroscience letters
547
59
64
https://tsukuba.repo.nii.ac.jp/record/29278/files/NeuLet_547.pdf
application/pdf
522.1 kB
2013-12-25