Related Experiment Video
Updated: Jul 8, 2026
07:47
Directly Measuring Forces Within Reconstituted Active Microtubule Bundles
Published on: May 10, 2022
CLASP-dependent microtubule stabilization generates microtubule-based protrusive forces during Drosophila epithelial
Sayani Sarkar1, Anna Pawluchin2, Anastasiia Sokolova2
1Institute of Cell Biology, ZMBE, Medical Faculty, University of Münster, Von-Esmarch-Straße 56, 48149 Münster, Germany; "Cells in Motion" Interfaculty Centre, University of Münster, Röntgenstraße 16, 48149 Münster, Germany.
Current Biology : CB
|July 6, 2026
Summary
Drosophila Orbit protein stabilizes dynamic microtubules, enabling them to withstand mechanical forces during tissue development. This microtubule stabilization is crucial for epithelial cell shape and tissue elongation.
Area of Science:
- Cell Biology
- Developmental Biology
- Biophysics
Background:
- Tissue morphogenesis relies on integrating biochemical signals and mechanical forces.
- Microtubules are increasingly recognized for their role in tissue remodeling, but their force-generating mechanisms in vivo are not fully understood.
- Dynamic microtubule plus ends are prone to catastrophes, limiting their load-bearing capacity.
Purpose of the Study:
- To investigate the role of microtubule dynamics in generating forces during tissue morphogenesis.
- To identify factors that stabilize microtubule plus ends in vivo.
- To elucidate the mechanism by which microtubules contribute to epithelial remodeling.
Main Methods:
- Utilized Drosophila pupal wing epithelium as a model system.
- Investigated the function of Orbit, a cytoplasmic linker-associated protein (CLASP) homolog.
- Analyzed microtubule stability, dynamics, and mechanical load-bearing capacity using live imaging and genetic manipulation.
- Examined the impact of Orbit on cell shape, tissue elongation, and protrusion formation.
Main Results:
- Identified Orbit as a key factor stabilizing non-centrosomal microtubule plus ends in vivo.
- Orbit-stabilized microtubules counteract actomyosin contractility and promote epithelial elongation.
- Loss of Orbit increases microtubule catastrophe frequency and disrupts tissue elongation.
- Orbit overexpression enhances microtubule rescues, promoting cell anisotropy and tissue extension.
- Orbit-mediated stabilization induces actin-independent, microtubule-dependent protrusions.
Conclusions:
- CLASP-dependent microtubule stabilization is a critical mechanism linking microtubule polymerization dynamics to epithelial morphogenesis.
- Orbit stabilizes microtubules, allowing them to sustain mechanical loads essential for tissue shaping.
- This study reveals a novel role for microtubule mechanics in driving tissue elongation and cell shape changes.
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