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Angiomotin cleavage promotes leader formation and collective cell migration
Yu Wang1, Yebin Wang1, Yuwen Zhu1
1Institute of Pediatrics, Children's Hospital of Fudan University and The Shanghai Key Laboratory of Medical Epigenetics, The International Co-laboratory of Medical Epigenetics and Metabolism, The State Key Laboratory of Genetic Engineering, Institutes of Biomedical Sciences, Shanghai Medical College of Fudan University, Shanghai 200032, China.
Developmental Cell
|October 10, 2024
Summary
Cleavage of angiomotin (AMOT) generates leader cells during collective cell migration (CCM). This process regulates focal adhesion maturation and tissue fluidity, crucial for embryonic development and cancer invasion.
Area of Science:
- Cell Biology
- Developmental Biology
- Cancer Biology
Background:
- Collective cell migration (CCM) is vital for embryonic development, angiogenesis, and cancer invasion.
- The molecular mechanisms driving CCM, particularly leader cell formation, remain incompletely understood.
Purpose of the Study:
- To elucidate the role of angiomotin (AMOT) cleavage in regulating collective cell migration and leader cell formation.
- To investigate how AMOT cleavage influences cell-matrix interactions and tissue dynamics.
Main Methods:
- Utilized mammalian epithelial cell cultures and mouse models.
- Investigated the localization and function of full-length AMOT and its C-terminal fragment (AMOT-CT).
- Analyzed focal adhesion maturation, traction force generation, and tissue fluidization.
Main Results:
- Full-length AMOT at cell junctions restricts motility; its cleavage is essential for CCM.
- Cleaved AMOT-CT promotes focal adhesion maturation and traction force at the cell-matrix interface.
- AMOT cleavage induces leader cell formation and coherent migration of cell collectives.
Conclusions:
- AMOT cleavage acts as a molecular switch, initiating polarized contraction.
- This switch promotes leader cell formation and drives collective cell migration.
- Understanding AMOT's role offers insights into embryonic morphogenesis and cancer invasion.
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