AMPK interacts with DSCAM and plays an important role in netrin-1 induced neurite outgrowth

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Kun Zhu, Xiaoping Chen, Jianghong Liu, Haihong Ye, Li Zhu, Jane Y Wu

  • Protein Cell
  • 2013
  • 13.6
  • 2013 Feb;4(2):155-61.
  • 10.1007/s13238-012-2126-2
  • 神经

Abstract

Down syndrome cell adhesion molecule (DSCAM) acts as a netrin-1 receptor and mediates attractive response of axons to netrin-1 in neural development. However, the signaling mechanisms of netrin-DSCAM remain unclear. Here we report that AMP-activated protein kinase (AMPK) interacts with DSCAM through its γ subunit, but does not interact with DCC (deleted in colorectal cancer), another major receptor for netrin-1. Netrin-treatment of cultured cortical neurons leads to increased phosphorylation of AMPK. Both AMPK mutant with dominant-negative effect and AMPK inhibitor can significantly suppress netrin-1 induced neurite outgrowth. Together, these findings demonstrate that AMPK interacts with DSCAM and plays an important role in netrin-1 induced neurite outgrowth. Our study uncovers a previously unknown component, AMPK, in netrin-DSCAM signaling pathway.
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