EPH/EPHRIN regulates cellular organization by actomyosin contractility effects on cell contacts
Abigail A Kindberg1,2,3,4,5, Vasudha Srivastava6, Jonathon M Muncie7,8,9,10
1Program in Craniofacial Biology, University of California, San Francisco, San Francisco, CA.
EPH/EPHRIN signaling drives cell self-organization by increasing actomyosin contractility, which reduces cell-cell contact stability. This mechanism, independent of cell migration, governs tissue organization through interfacial tension.
Area of Science:
- Cell Biology
- Biophysics
- Developmental Biology
Background:
- EPH/EPHRIN signaling is crucial for tissue development and morphogenesis.
- The precise role of cell mechanics in EPH/EPHRIN-mediated self-organization remains unclear.
Purpose of the Study:
- To investigate how EPH/EPHRIN signaling influences cell mechanics.
- To elucidate the biomechanical mechanisms underlying EPH/EPHRIN-driven cell segregation and tissue self-organization.
Main Methods:
- Contact angle measurements to assess cell:cell contact stability.
- Atomic force microscopy and live cell imaging to analyze cortical tension and myosin localization.
- Cell aggregate experiments and mouse genetics to study tissue organization.
Main Results:
- EPH/EPHRIN signaling increases cortical actomyosin contractility, decreasing heterotypic cell:cell contact stability.
- Cell segregation is driven by actomyosin contractility, independent of directed migration or altered cell adhesion.
- Increased actomyosin contractility also promotes homotypic EPHB2:EPHB2 contacts and drives tissue reorganization by minimizing heterotypic contacts.
Conclusions:
- EPH/EPHRIN signaling regulates cell mechanics via actomyosin contractility to drive cell segregation.
- Differences in interfacial tension, modulated by actomyosin contractility, are key to EPH/EPHRIN-based cellular self-organization and tissue patterning.
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