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Purification and Analysis of Caenorhabditis elegans Extracellular Vesicles
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Secreted exosomes induce filopodia formation.

Caitlin McAtee1,2, Mikin Patel3, Daisuke Hoshino4

  • 1Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, USA.

Biorxiv : the Preprint Server for Biology
|March 31, 2025
PubMed
Summary
This summary is machine-generated.

Secreted exosomes, particularly small EVs (SEVs), drive filopodia formation. Cancer cell-derived SEVs use endoglin and THSD7A, while neuronal SEVs use THSD7A to promote filopodia and synapse formation via Cdc42 activation.

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Area of Science:

  • Cell Biology
  • Extracellular Vesicles
  • Cytoskeletal Dynamics

Background:

  • Filopodia are crucial for cell sensing, adhesion, migration, and neuronal synapse formation.
  • Actin cytoskeleton dynamics are key to filopodia, but upstream extracellular signals remain largely unknown.

Purpose of the Study:

  • To identify upstream extracellular regulators of filopodia formation.
  • To elucidate the role of exosomes in filopodia biogenesis and function.

Main Methods:

  • Inhibition of exosome secretion and rescue experiments with purified extracellular vesicles (EVs).
  • Proteomic analysis of small EVs (SEVs) from cancer cells and endoglin-knockdown cells.
  • Functional assays assessing filopodia formation, cancer cell metastasis, neuronal migration, and synapse formation.

Main Results:

  • Exosome secretion inhibition impaired filopodia and synapse formation in cancer cells and neurons.
  • Small EVs (SEVs) demonstrated potent filopodia-inducing activity.
  • Cancer cell SEVs utilize endoglin and THSD7A; neuronal SEVs utilize THSD7A to promote filopodia via Cdc42 activation.

Conclusions:

  • Secreted exosomes, specifically SEVs carrying THSD7A, represent a novel signaling mechanism for filopodia formation.
  • This exosome-mediated pathway is critical for both cancer cell metastasis and neuronal synapse development.