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Evidence for a second cell cycle block at G2/M by p53
N Stewart1, G G Hicks, F Paraskevas
1Manitoba Institute of Cell Biology, Manitoba Cancer Treatment and Research Foundation, Winnipeg, Canada.
Oncogene
|January 5, 1995
Summary
Wild type p53 induces cell cycle arrest. Mutant p53, when co-expressed with H-ras, also causes cell cycle arrest at G1/S and G2/M, suggesting p53
Area of Science:
- Molecular Biology
- Cell Biology
- Cancer Research
Background:
- Wild type p53 protein is known to arrest the cell cycle at G1/S.
- Most p53 mutants lose this cell cycle arrest ability.
- Previous studies showed p53 mutants can rescue cells from ras-induced arrest, while wild type p53 inhibits growth.
Purpose of the Study:
- To investigate if p53 can induce cell cycle arrest at the G2/M boundary.
- To analyze the role of p53 in cell cycle regulation at different checkpoints.
Main Methods:
- Utilized the REF52 cell line.
- Employed a temperature-sensitive p53val135 mutant allele.
- Enriched cells in late G1/early S phases before temperature shift.
- Analyzed cell cycle progression using flow cytometry.
Main Results:
- REF52 cells expressing mutant p53val135 and activated H-ras arrested at both G1/S and G2/M phases at the restrictive temperature.
- Flow cytometry confirmed these cell cycle arrest points.
Conclusions:
- p53's anti-proliferative activity is involved in regulating the G2/M checkpoint.
- p53 also plays a role in G1/S transit and DNA synthesis initiation.
- These findings highlight p53's multifaceted role in cell cycle control.