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Updated: Sep 1, 2025

A Time-Efficient Fluorescence Spectroscopy-Based Assay for Evaluating Actin Polymerization Status in Rodent and Human Brain Tissues
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A Time-Efficient Fluorescence Spectroscopy-Based Assay for Evaluating Actin Polymerization Status in Rodent and Human Brain Tissues

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Vav independently regulates synaptic growth and plasticity through distinct actin-based processes

Hyun Gwan Park1,2, Yeongjin David Kim1,2, Eunsang Cho1,2

  • 1Department of Brain and Cognitive Sciences, Seoul National University, Seoul, Korea.

The Journal of Cell Biology
|August 17, 2022
PubMed

Insights

The Vav-Rac1-SCAR pathway regulates synaptic growth and plasticity by controlling actin dynamics. This pathway is crucial for macropinocytosis and reserve pool vesicle mobilization at the Drosophila NMJ.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Molecular Biology

Background:

  • Presynaptic actin dynamics are key to synaptic growth and plasticity.
  • The Rac1-SCAR pathway in Drosophila NMJs mediates BMP-induced macropinocytosis, inhibiting BMP growth signaling.

Purpose of the Study:

  • To investigate the role of the Rho-type GEF Vav upstream of Rac1 in synaptic growth and plasticity.
  • To elucidate the mechanisms by which Vav-Rac1-SCAR signaling regulates structural and functional presynaptic plasticity.

Main Methods:

  • Utilized Drosophila NMJs as a model system.
  • Investigated the function of Vav, Rac1, and SCAR in synaptic plasticity and macropinocytosis.
  • Assessed post-tetanic potentiation (PTP) and synaptic depression.
  • Examined reserve pool (RP) vesicle mobilization.
  • Used F-actin-stabilizing drugs to rescue defects in Vav mutants.

Main Results:

  • Vav acts upstream of Rac1 to inhibit synaptic growth via macropinocytosis.
  • Vav-Rac1-SCAR signaling is essential for tetanus-induced synaptic plasticity, affecting PTP and synaptic depression.
  • Impairment of this pathway disrupts reserve pool (RP) vesicle mobilization.
  • F-actin stabilization rescues RP mobilization and plasticity defects in Vav mutants.

Conclusions:

  • The actin-regulatory Vav-Rac1-SCAR signaling pathway independently controls structural and functional presynaptic plasticity.
  • This pathway regulates macropinocytosis for structural plasticity and RP mobilization for functional plasticity.

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