Spef1 is a microvillar component that limits apical actomyosin contractility and preserves intestinal barrier
Rocio Tapia1, Angelo Morales1, Gail A Hecht2
1Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, TN 37232, US.
Current Biology : CB
|January 17, 2026
Summary
Sperm Flagellar 1 (Spef1) prevents excessive actomyosin contractility in epithelial cells. Loss of Spef1 leads to apical invaginations and compromised barrier function by increasing tension.
Area of Science:
- Cell Biology
- Epithelial Biology
- Biophysics
Background:
- Epithelial integrity relies on cell-cell contacts reinforced by actomyosin contractility.
- Tension regulation is crucial for maintaining barrier function without compromising physical properties.
Purpose of the Study:
- To investigate the role of Sperm Flagellar 1 (Spef1) in regulating actomyosin contractility and epithelial barrier function.
- To understand how epithelial cells tune apical tension for junctional reinforcement.
Main Methods:
- Utilized Caco-2 BBE cell models with Spef1 loss-of-function.
- Analyzed apical domain morphology, junctional component distribution, and actomyosin tension.
- Investigated the role of NM2A:NM2C heavy chain ratio in tension regulation.
Main Results:
- Spef1 deficiency caused apical domain invaginations at tricellular contacts.
- Loss of Spef1 led to redistribution of tricellular and tight junction components.
- Increased NM2A:NM2C heavy chain ratio elevated apical tension and impaired barrier function.
Conclusions:
- Spef1, a microvillar protein, acts as a crucial regulator preventing actomyosin hypercontractility.
- Spef1 tunes apical surface tension for appropriate junctional reinforcement and epithelial function maintenance.
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