14-3-3ε and NAV2 interact to regulate neurite outgrowth and axon elongation

Mark A. Marzinke, Terri Mavencamp, Joseph Duratinsky, Margaret Clagett-Dame

Research output: Contribution to journalArticle

Abstract

Neuron navigator 2 (NAV2) is required for all-trans retinoic acid (atRA) to induce neurite outgrowth in human neuroblastoma cells. Further, ectopic overexpression of full-length human NAV2 rescues an axonal elongation defect in the Caenorhabditis elegans unc-53 (NAV2 ortholog) mutant. Using a region of NAV2 that independently associates with the cytoskeleton as bait in a yeast-two-hybrid screen, 14-3-3ε was identified as a novel NAV2 interacting partner. Amino acids 761-960 of NAV2 are sufficient to confer a positive interaction with 14-3-3ε as evidenced by a two-hybrid screen and co-immunoprecipitation assay. Knockdown of 14-3-3ε leads to a decrease in atRA-mediated neurite outgrowth, similar to the elongation defects observed when NAV2 is depleted or mutated. Likewise, posterior lateral microtubule (PLM) defects in C. elegans fed unc-53 RNAi are similar to those fed ftt-2 (14-3-3 homolog) RNAi. The discovery of an interaction between NAV2 and 14-3-3ε could provide insight into the mechanism by which NAV2 participates in promoting cell migration and neuronal elongation.

Original languageEnglish (US)
Pages (from-to)94-100
Number of pages7
JournalArchives of Biochemistry and Biophysics
Volume540
Issue number1-2
DOIs
StatePublished - Nov 13 2013
Externally publishedYes

Keywords

  • 14-3-3ε
  • Axon elongation
  • NAV2
  • Neuron navigator 2
  • UNC-53
  • YWHAE

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology

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