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p300 regulates p63 transcriptional activity.
Mary MacPartlin1, Shelya Zeng, Hunjoo Lee
1Department of Biochemistry and Molecular Biology, Oregon Health and Science University, Portland, Oregon 97239, USA.
The Journal of Biological Chemistry
|June 21, 2005
Summary
The transcriptional co-activator p300 regulates the tumor suppressor p63. p300 stimulates p63-dependent transcription of p21, leading to cell cycle arrest.
Area of Science:
- Molecular Biology
- Cell Biology
- Cancer Research
Background:
- The transcriptional co-activator p300 is known to regulate tumor suppressors p53 and p73.
- The role of p300 in regulating the p63 family, particularly p63gamma, remains less understood.
Purpose of the Study:
- To investigate the interaction between p300 and p63gamma.
- To determine the effect of p300 on p63gamma-mediated transcriptional activity and downstream targets like p21.
- To elucidate the functional consequences of p300-p63gamma interaction on cell cycle regulation.
Main Methods:
- In vitro binding assays to assess p300 and p63gamma interaction.
- Cell-based assays to evaluate transcriptional activity and p21 induction.
- Analysis of p300 acetylase-defective mutant (AT2) and deltaN-p63gamma isoform effects.
Main Results:
- p300 directly binds to the N-terminal domain of p63gamma, and vice versa, in vitro and in cells.
- p300, but not its acetylase-defective mutant AT2, enhances p63gamma-dependent transcription and p21 induction.
- The deltaN-p63gamma isoform and p300AT2 inhibit p63gamma-induced p21 expression.
Conclusions:
- p300 acts as a crucial regulator of p63-dependent transcription.
- p300's HAT activity is essential for its co-activation function on p63gamma.
- p300-p63gamma interaction influences p21 expression and cell cycle G1 arrest.
