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Aurora B-mediated abscission checkpoint protects against tetraploidization
Patrick Steigemann1, Claudia Wurzenberger, Michael H A Schmitz
1Institute of Biochemistry, Swiss Institute of Technology Zurich, ETHZ, Zurich, Switzerland.
Cell
|February 11, 2009
Summary
A novel cell division control mechanism prevents cancer-promoting tetraploidization in human cells. Aurora B kinase activity, regulated by chromosome segregation, ensures proper cell division and suppresses abnormal cell growth.
Area of Science:
- Cell Biology
- Genetics
- Cancer Research
Background:
- Genomic abnormalities, including tetraploidization, are hallmarks of cancer and arise from failed cytokinesis.
- Tetraploidization is considered an early event in cancer development, highlighting the need to understand its prevention mechanisms.
Purpose of the Study:
- To elucidate a cell division control mechanism that prevents tetraploidization in human cells with errors in chromosome segregation.
- To investigate the role of Aurora B kinase in regulating cytokinesis and preventing tetraploidization.
Main Methods:
- Analysis of human cells with perturbed chromosome segregation.
- Investigating the activity of Aurora B kinase during cell division.
- Studying the phosphorylation of mitotic kinesin-like protein 1 (Mklp1).
Main Results:
- Aurora B inactivation was found to promote the completion of cytokinesis by abscission.
- Chromosome bridges maintained Aurora B activity, delaying abscission and preventing tetraploidization via furrow regression.
- A pathway involving Aurora B and Mklp1 phosphorylation was identified as crucial for suppressing tetraploidization.
Conclusions:
- Aurora B acts as a sensor for unsegregated chromatin at the cleavage site during cell division.
- Cell abscission is tightly coordinated with chromosome segregation completion in human cells to prevent tetraploidization.
- This mechanism protects against cancer formation by maintaining genomic stability.
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