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Roles of aurora-A kinase in mitotic entry and G2 checkpoint in mammalian cells
Tomotoshi Marumoto1, Toru Hirota, Tetsuro Morisaki
1Department of Tumor Genetics and Biology, Kumamoto University School of Medicine, 2-2-1 Honjo, Kumamoto 860-0811, Japan.
Background:
Various mitotic events are controlled by Cdc2-cyclin B and other mitotic kinases. Aurora/Ipl1-related mitotic kinases were proved to play key roles in mitotic progression in diverse lower organisms. Aurora-A is a mammalian counterpart of aurora/Ipl1-related kinases and is thought to be a potential oncogene. However, the regulation of aurora-A activation and the commitment of aurora-A in the progression of G2-M phase are largely unknown in mammalian cells.
Results:
We demonstrated that aurora-A is activated depending on the activation of Cdc2-cyclin B in mammalian cells. Since Cdc2-cyclin B does not directly phosphorylate aurora-A, indirect pathways such as the inhibition of PP1 by Cdc2-cyclin B may act for the activation of aurora-A kinase. Microinjection of anti-aurora-A antibodies into HeLa cells at late G2 phase caused a significant delay in mitotic entry. Furthermore, aurora-A activation at G2-M transition was inhibited by DNA damage, and the over-expression of aurora-A induced the abrogation of the DNA damage-induced G2 checkpoint.
Conclusions:
Aurora-A is activated downstream of Cdc2-cyclin B and plays crucial roles in proper mitotic entry and G2 checkpoint control. Dysregulation of aurora-A induces abnormal G2-M transition in mammalian cells and may lead to chromosome instability, which results in the development and progression of malignant tumours.
Insights
Aurora-A kinase activation is dependent on Cdc2-cyclin B, playing a key role in cell cycle progression and DNA damage checkpoints. Its dysregulation can lead to abnormal cell division and cancer.
Area of Science:
- Cell Biology
- Molecular Biology
- Cancer Research
Background:
- Mitotic events are regulated by Cdc2-cyclin B and other kinases.
- Aurora/Ipl1-related kinases are crucial for mitotic progression in lower organisms.
- Aurora-A, a mammalian counterpart, is a potential oncogene with unknown regulatory mechanisms in mammalian cells.
Purpose of the Study:
- To elucidate the regulation of aurora-A activation during the G2-M phase transition in mammalian cells.
- To investigate the role of aurora-A in mitotic entry and checkpoint control.
Main Methods:
- Demonstration of aurora-A activation dependency on Cdc2-cyclin B.
- Investigation of indirect activation pathways, such as PP1 inhibition.
- Microinjection of anti-aurora-A antibodies into HeLa cells.
- Analysis of aurora-A activation under DNA damage conditions and the effect of aurora-A overexpression on the G2 checkpoint.
Main Results:
- Aurora-A activation is dependent on Cdc2-cyclin B activation, likely through indirect mechanisms.
- Inhibition of aurora-A delays mitotic entry.
- DNA damage inhibits aurora-A activation at G2-M transition.
- Overexpression of aurora-A abrogates the DNA damage-induced G2 checkpoint.
Conclusions:
- Aurora-A is activated downstream of Cdc2-cyclin B and is essential for accurate mitotic entry.
- Aurora-A plays a critical role in G2 checkpoint control.
- Dysregulation of aurora-A contributes to abnormal G2-M transition, genomic instability, and potentially cancer development.
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