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JCS ePress
online publication date 28 Sep 2004
doi: 10.1242/jcs.01384
Research Article
p73 competes with co-activators and recruits histone deacetylase to NF-Y in the repression of PDGF 
-receptor
Hidetaka Uramoto,
Daniel Wetterskog,
Anders Hackzell,
Yoshiki Matsumoto,
and
Keiko Funa*
* Author for correspondence (e-mail: keiko.funa{at}anatcell.gu.se)
We investigated mechanisms of the p73
-mediated repression of the platelet-derived growth factor 
-receptor (PDGFRB) promoter caused by its interaction with NF-Y. Treatment of cells with the histone deacetylase (HDAC) inhibitor, Trichostatin A, increases PDGFRB promoter activity through the CCAAT motif and counteracts the repression caused by p73. Activation of the PDGFRB promoter by the co-activator p300 also occurs through the CCAAT motif. Expression of p73 counteracts both p300- and P/CAF-mediated activation of the PDGFRB promoter, and expression of p300 or P/CAF attenuates the p73-mediated repression of the promoter activity. In concordance, p73 decreases the p300-mediated acetylation of NF-YC, p300 competes with p73 for binding NF-YB, and P/CAF competes with p73 for binding NF-YB and NF-YC. Furthermore, p73, but not the oncogenic 
Np73, binds directly to HDAC1. We performed chromatin immunoprecipitation with antibodies against p73, Np73, NFYB, p300 and HDAC1 at different periods after serum stimulation in serum-starved NIH3T3 cells. A marked decrease of Np73, NF-YB and p300 was detected 6 hours after serum stimulation when the expression of PDGFRB decreased. Conversely, HDAC1 was found bound at its maximum and the anti-p73 detecting both TAp73 and Np73 was found at all time points, indicating that p73, but not Np73, remains bound at this time. Double immunofluorescence staining of TAp73 and HDAC1 revealed that both of these molecules exist in the nucleus at this time point, supporting the presence of endogenous interaction. These results suggest that p73 and Np73 behave as physiological regulators for the transcription of the PDGFRB promoter.
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© The Company of Biologists Ltd 2004
