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Cortical microtubules oppose actomyosin-driven membrane ingression during
Alyssa R Quiogue1, Eisuke Sumiyoshi1, Adam Fries1,2
1Institute of Molecular Biology.
Biorxiv : the Preprint Server for Biology
|June 9, 2023
Summary
Microtubule stability, regulated by CLS-2 and kinetochore proteins like KNL-1 and BUB-1, is crucial for C. elegans oocyte meiosis I. This stability limits membrane ingression, enabling proper contractile ring assembly and polar body extrusion.
Area of Science:
- Cell Biology
- Developmental Biology
- Molecular Biology
Background:
- During C. elegans oocyte meiosis I, a contractile ring assembles within a larger cortical actomyosin network.
- This network mediates ring dynamics and controls membrane ingression during polar body extrusion.
- CLS-2, a microtubule-stabilizing protein, was previously proposed to balance actomyosin tension and microtubule stiffness for ring assembly.
Approach:
- Live cell imaging and fluorescent protein fusions were used to study CLS-2 and associated proteins.
- The functions of CLS-2, KNL-1, and BUB-1 were investigated by reducing their activity.
- Microtubule stability was manipulated using nocodazole and taxol treatments.
Key Points:
- CLS-2, KNL-1, and BUB-1 are part of a kinetochore protein complex co-localizing to cortical patches during oocyte meiosis I.
- These proteins are essential for cortical microtubule stability, limiting membrane ingression, and facilitating polar body extrusion.
- Altering microtubule stability (destabilization or stabilization) directly impacts membrane ingression and polar body extrusion success.
Conclusions:
- CLS-2, as part of a kinetochore sub-complex, stabilizes microtubules to stiffen the oocyte cortex.
- This cortical stiffening limits overall membrane ingression, crucial for contractile ring function.
- Successful polar body extrusion during meiosis I relies on this balance of microtubule-mediated stiffness and actomyosin dynamics.
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