NGF-induced axon growth is mediated by localized inactivation of GSK-3β and functions of the microtubule plus end binding protein APC

Feng Quan Zhou, Jiang Zhou, Shoukat Dedhar, Yao Hong Wu, William D. Snider

Research output: Contribution to journalArticlepeer-review

Abstract

Little is known about how nerve growth factor (NGF) signaling controls the regulated assembly of microtubules that underlies axon growth. Here we demonstrate that a tightly regulated and localized activation of phosphatidylinositol 3-kinase (PI3K) at the growth cone is essential for rapid axon growth induced by NGF. This spatially activated PI3K signaling is conveyed downstream through a localized inactivation of glycogen synthase kinase 3β (GSK-3β). These two spatially coupled kinases control axon growth via regulation of a microtubule plus end binding protein, adenomatous polyposis coli (APC). Our results demonstrate that NGF signals are transduced to the axon cytoskeleton via activation of a conserved cell polarity signaling pathway.

Original languageEnglish (US)
Pages (from-to)897-912
Number of pages16
JournalNeuron
Volume42
Issue number6
DOIs
StatePublished - Jun 24 2004
Externally publishedYes

ASJC Scopus subject areas

  • Neuroscience(all)

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