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Collective chemotaxis requires contact-dependent cell polarity
Eric Theveneau1, Lorena Marchant, Sei Kuriyama
1Department of Cell and Developmental Biology, University College London, London WC1E 6BT, UK.
Developmental Cell
|July 21, 2010
Summary
Chemokines like Sdf1 guide collective cell migration by stabilizing cell protrusions at cell contacts. This mechanism, involving N-cadherin and Rac1, is crucial for embryogenesis and cancer metastasis.
Area of Science:
- Cell Biology
- Developmental Biology
- Cancer Biology
Background:
- Directional collective cell migration is vital in embryogenesis and cancer progression.
- The precise mechanisms by which cell clusters respond to chemoattractants remain incompletely understood.
- Neural crest cells exhibit high motility, with behaviors mirroring malignant invasion.
Purpose of the Study:
- To investigate how neural crest cells collectively respond to the chemokine Sdf1.
- To elucidate the molecular mechanisms underlying Sdf1-mediated directional cell migration.
- To understand the role of N-cadherin in contact inhibition of locomotion and chemoattraction.
Main Methods:
- Live imaging of neural crest cell migration in response to Sdf1.
- Analysis of cell protrusion dynamics and Rac1 activity.
- Investigating the interplay between N-cadherin, cell-cell contacts, and migratory behavior.
Main Results:
- Neural crest cells exhibit collective attraction towards Sdf1.
- Sdf1 stabilizes cell protrusions at cell contacts, promoting directional migration.
- N-cadherin at cell contacts inhibits protrusions and Rac1, while promoting them at the free edge.
Conclusions:
- Sdf1 amplifies and stabilizes contact-dependent cell polarity, driving directional collective migration.
- N-cadherin plays a role in contact inhibition of locomotion.
- The identified mechanism is relevant to both embryonic development and cancer metastasis.
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