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RINGO C is required to sustain the spindle-assembly checkpoint
Silvana Mourón1, Guillermo de Cárcer, Esther Seco
1Signalling and Cell Cycle Group, CNIO (Spanish National Cancer Center), Melchor Fernández Almagro 3, 28029 Madrid, Spain.
Journal of Cell Science
|July 8, 2010
Summary
RINGO C protein is crucial for the spindle-assembly checkpoint (SAC) and proper chromosome segregation during cell division. Its depletion causes premature mitotic exit and defects in SAC component recruitment and Aurora B kinase activity.
Area of Science:
- Cell Biology
- Molecular Biology
- Genetics
Background:
- RINGO/Speedy proteins are Cdk1/Cdk2 activators lacking cyclin homology.
- Their precise roles in cell-cycle regulation require further elucidation.
Purpose of the Study:
- To characterize the function of the human RINGO C protein in cell-cycle progression.
- To investigate its role in the spindle-assembly checkpoint (SAC) and mitotic fidelity.
Main Methods:
- siRNA-mediated knockdown of RINGO C.
- Time-lapse microscopy.
- Analysis of spindle-assembly checkpoint (SAC) component recruitment (Mad2, Bub1, BubR1).
- Assessment of chromosome segregation and Aurora B kinase activity.
Main Results:
- RINGO C depletion leads to premature mitotic exit and chromosome misalignment, even with microtubule poisons.
- RINGO C is involved in the spindle-assembly checkpoint (SAC), with depleted cells showing impaired recruitment of SAC components.
- Cells lacking RINGO C exhibit defective chromosome segregation, increased micronuclei, and binucleated structures.
- RINGO C associates with Aurora B kinase, and its downregulation causes mislocalization of active Aurora B.
Conclusions:
- RINGO C plays a critical role in maintaining the mitotic checkpoint.
- Its function may involve facilitating SAC component recruitment and regulating Aurora B kinase activity.
- Defects in RINGO C function lead to mitotic errors and genomic instability.
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