Neurotrophins and netrins require calcineurin/NFAT signaling to stimulate outgrowth of embryonic axons.

Published

Journal Article

Axon outgrowth is the first step in the formation of neuronal connections, but the pathways that regulate axon extension are still poorly understood. We find that mice deficient in calcineurin-NFAT signaling have dramatic defects in axonal outgrowth, yet have little or no defect in neuronal differentiation or survival. In vitro, sensory and commissural neurons lacking calcineurin function or NFATc2, c3, and c4 are unable to respond to neurotrophins or netrin-1 with efficient axonal outgrowth. Neurotrophins and netrins stimulate calcineurin-dependent nuclear localization of NFATc4 and activation of NFAT-mediated gene transcription in cultured primary neurons. These data indicate that the ability of these embryonic axons to respond to growth factors with rapid outgrowth requires activation of calcineurin/NFAT signaling by these factors. The precise parsing of signals for elongation turning and survival could allow independent control of these processes during development.

Full Text

Duke Authors

Cited Authors

  • Graef, IA; Wang, F; Charron, F; Chen, L; Neilson, J; Tessier-Lavigne, M; Crabtree, GR

Published Date

  • May 30, 2003

Published In

Volume / Issue

  • 113 / 5

Start / End Page

  • 657 - 670

PubMed ID

  • 12787506

Pubmed Central ID

  • 12787506

International Standard Serial Number (ISSN)

  • 0092-8674

Digital Object Identifier (DOI)

  • 10.1016/s0092-8674(03)00390-8

Language

  • eng

Conference Location

  • United States