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Related Experiment Video

Updated: May 20, 2026

Traction Microscopy Integrated with Microfluidics for Chemotactic Collective Migration

Traction Microscopy Integrated with Microfluidics for Chemotactic Collective Migration

Published on: October 13, 2019

Evi5 promotes collective cell migration through its Rab-GAP activity.

Carl Laflamme¹, Gloria Assaker, Damien Ramel

¹Institute for Research in Immunology and Cancer, University of Montréal, Montréal, Québec, Canada.

The Journal of Cell Biology

|July 11, 2012

Summary

Researchers identified Evi5, a novel regulator of membrane trafficking, essential for collective cell migration in Drosophila border cells. Evi5 controls Rab11 activity, impacting guidance receptor polarization and cell movement.

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Area of Science:

Cell Biology
Developmental Biology
Molecular Biology

Background:

Membrane trafficking is crucial for cell migration, but its regulatory mechanisms remain unclear.
Collective cell migration, exemplified by Drosophila border cells, provides a model to study these processes.

Purpose of the Study:

To identify novel regulators of membrane trafficking during collective cell migration.
To elucidate the molecular mechanism of Evi5 in controlling cell migration.

Main Methods:

Conducted a screen for Rab-GTPase-activating proteins (GAPs) in Drosophila border cell migration.
Utilized genetic manipulation to study the function of the uncharacterized protein Evi5.
Investigated the interaction between Evi5 and Rab11 GTPase.

Main Results:

Identified Evi5 as a key regulator of membrane trafficking in Drosophila border cells.
Demonstrated that Evi5 functions as a GTPase-activating protein (GAP) for Rab11.
Showed that both loss and gain of Evi5 function impair border cell migration by disrupting Rab11-dependent receptor polarization.

Conclusions:

Evi5 is an essential regulator of collective cell migration through its Rab-GAP activity on Rab11.
Disruption of Evi5-Rab11 signaling impairs guidance receptor polarization, affecting cell migration.
Findings enhance understanding of endocytosis and cell signaling regulation during migration.