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Updated: Jul 6, 2026
06:29
Real-Time Monitoring of Aurora kinase A Activation using Conformational FRET Biosensors in Live Cells
Published on: July 30, 2020
Id1 overexpression induces tetraploidization and multiple abnormal mitotic phenotypes by modulating aurora A.
Cornelia Man1, Jack Rosa, Y L Yip
1Department of Anatomy, The University of Hong Kong, Pokfulam, Hong Kong SAR, China.
Molecular Biology of the Cell
|March 21, 2008
Summary
The transcription factor Id1 induces cell division errors, causing tetraploidy by stabilizing Aurora A. Id1 interferes with Aurora A degradation by binding Cdh1, a key protein in the cell cycle regulation pathway.
Area of Science:
- Cell Biology
- Molecular Biology
- Cancer Research
Background:
- The transcription factor Id1 plays a role in cell proliferation and differentiation.
- Mitotic errors can lead to genomic instability and diseases like cancer.
- Aurora A kinase is a key regulator of mitosis, and its overexpression is linked to various cancers.
Purpose of the Study:
- To investigate the role of Id1 in inducing tetraploidy and mitotic aberrations.
- To elucidate the mechanism by which Id1 affects Aurora A stability.
- To explore the interaction between Id1, Aurora A, and the APC/C(Cdh1) complex.
Main Methods:
- Generation of transient and stable Id1-expressing cell models.
- Microscopic analysis of mitotic aberrations (centrosome amplification, binucleation, spindle defects).
- Western blotting and co-immunoprecipitation to assess protein levels and interactions.
- RNA interference to knock down Aurora A expression.
- Analysis of Aurora A promoter activity and degradation pathways.
Main Results:
- Id1 overexpression induced tetraploidy and multiple mitotic aberrations in nasopharyngeal epithelial cells.
- Id1 stabilized Aurora A protein levels, and Aurora A knockdown partially rescued Id1-induced mitotic defects.
- Id1 did not involve DNA amplification or significant transcriptional activation of Aurora A.
- Id1 was found to bind to Cdh1, a component of the anaphase-promoting complex/cyclosome (APC/C).
- This Id1-Cdh1 interaction interfered with Cdh1's ability to target Aurora A for degradation, leading to Aurora A stabilization.
Conclusions:
- Id1 induces tetraploidy and mitotic defects by stabilizing Aurora A.
- Id1 stabilizes Aurora A by disrupting the APC/C(Cdh1)-mediated degradation pathway through direct interaction with Cdh1.
- These findings reveal a novel mechanism linking Id1 to cell cycle regulation and genomic instability.
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