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Nudel binds Cdc42GAP to modulate Cdc42 activity at the leading edge of migrating cells

Yidong Shen1, Ning Li, Shuang Wu

  • 1Laboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 320 Yue Yang Road, Shanghai 200031, China.

Developmental Cell
|March 12, 2008
PubMed

Insights

Nudel regulates cell migration by controlling Cdc42 inactivation. It sequesters Cdc42GAP at the cell's leading edge, stabilizing active Cdc42 and promoting migration.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Cell migration is crucial for development and disease.
  • Cdc42 GTPase activation at the leading edge drives cell migration.
  • Regulation of Cdc42 GTPase-activating protein (Cdc42GAP) is poorly understood.

Purpose of the Study:

  • To investigate the regulation of Cdc42GAP.
  • To identify novel regulators of Cdc42 GTPase activity during cell migration.
  • To elucidate the role of Nudel in cell migration.

Main Methods:

  • Co-immunoprecipitation assays to study protein interactions.
  • RNA interference (RNAi) to deplete Nudel.
  • Confocal microscopy to analyze protein localization.
  • Site-directed mutagenesis to create nonphosphorylatable Nudel mutants.

Main Results:

  • Nudel competes with Cdc42 for binding to Cdc42GAP, inhibiting Cdc42GAP activity.
  • Nudel and Cdc42GAP localize to the leading edge of migrating cells.
  • Nudel's leading-edge localization depends on Erk1/2 phosphorylation.
  • Nudel depletion or expression of nonphosphorylatable Nudel impairs Cdc42 activation and cell migration.

Conclusions:

  • Nudel acts as a novel regulator of Cdc42 during cell migration.
  • Nudel facilitates cell migration by sequestering Cdc42GAP, stabilizing active Cdc42 at the leading edge.
  • Nudel's phosphorylation by Erk1/2 is essential for its function in cell migration.

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