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The NESH/Abi-3-based WAVE2 complex is functionally distinct from the Abi-1-based WAVE2 complex.

Saki Sekino1, Yuriko Kashiwagi2, Hitoshi Kanazawa3

  • 1School of Life Sciences, Tokyo University of Pharmacy and Life Sciences, Hachioji, Tokyo, 192-0392, Japan. pupa72040320@yahoo.co.jp.

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Summary
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The NESH/Abi-3 protein forms a WAVE2 complex distinct from Abi-1, impairing lamellipodial protrusions but promoting invadopodia formation in specific conditions. This highlights functional differences in Abl interactor (Abi) family proteins.

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Abl interactor (Abi) proteins are crucial for actin cytoskeleton organization via the WAVE complex.
  • Mammalian cells express three Abi proteins: Abi-1, Abi-2, and NESH/Abi-3.
  • Abi-1 interacts with c-Abl tyrosine kinase to mediate WAVE2 phosphorylation and actin remodeling.

Purpose of the Study:

  • To characterize NESH/Abi-3 and compare its functions with Abi-1 and Abi-2.
  • To investigate the role of NESH/Abi-3 in WAVE2 complex formation and cellular protrusions.
  • To elucidate the structural basis for c-Abl interaction with Abi proteins.

Main Methods:

  • Ectopic expression of NESH/Abi-3 in NIH3T3 cells.
  • Analysis of WAVE2 complex formation and cellular morphology on fibronectin.
  • Expression of Abi proteins in v-src-transformed NIH3T3 cells and treatment with Abl kinase inhibitors or siRNA.
  • Structural analysis of Abi-1 interaction with c-Abl.

Main Results:

  • NESH/Abi-3 expression led to endogenous Abi-1 degradation and formation of a NESH/Abi-3-based WAVE2 complex.
  • The NESH/Abi-3-based WAVE2 complex impaired WAVE2 translocation to the plasma membrane and lamellipodial protrusion.
  • NESH/Abi-3 expression, combined with c-Abl inhibition or knockdown, promoted invadopodia formation.
  • A specific linker region in Abi-1 is essential for c-Abl interaction and WAVE2 phosphorylation.

Conclusions:

  • The NESH/Abi-3-based WAVE2 complex exhibits distinct functions compared to the Abi-1-based complex.
  • NESH/Abi-3 plays a role in the formation of ventral protrusions under specific cellular conditions.