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Nucleic Acids Research Advance Access originally published online on October 25, 2007
Nucleic Acids Research 2007 35(21):7348-7359; doi:10.1093/nar/gkm870
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Nucleic Acids Research, 2007, Vol. 35, No. 21 7348-7359
© 2007 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-com

Molecular Biology

Negative regulation of transcription coactivator p300 by orphan receptor TR3

Gui-deng Li, Jin-xu Fang, Hang-zi Chen, Jie Luo, Zhong-hui Zheng, Yue-mao Shen and Qiao Wu*

Key Laboratory of the Ministry of Education for Cell Biology and Tumor Cell Engineering, School of Life Sciences, Xiamen University, Xiamen 361005, Fujian Province, China

* To whom correspondence should be addressed. Tel: +592 2187959; Fax: +592 2086630; Email: qiaow{at}xmu.edu.cn

Received June 22, 2007. Revised September 28, 2007. Accepted September 29, 2007.

p300 regulates the transcriptional activity of a variety of transcription factors by forming an activation complex and/or promoting histone acetylation. Here, we show a unique characteristic of orphan receptor TR3 in negatively regulating the function of p300. TR3 was found to interact with p300 and inhibited the acetylation of transcription factors induced by p300, resulting in the repression of their transcriptional activity. Further analysis revealed that both a conserved transcriptional adapter motif (TRAM) in p300 and a specific sequence FLELFIL in TR3 were critical for their interaction. TR3 binding completely covered the histone acetyltransferase (HAT) domain of p300 and resulted in suppression of the HAT activity, as the p300-induced histone H3 acetylation and transcription were inhibited with the presence TR3. Furthermore, an agonist of TR3, a natural octaketide isolated from Dothiorella sp. HTF3 of an endophytical fungus, was shown to be a potent compound for inhibiting p300 HAT activity (IC50 = 1.5 µg/ml) in vivo. More importantly, this agonist could repress the transcriptional activity of transcription factors, and proliferation of cancer cells. Taken together, our results not only delineate a novel transcriptional repressor function for TR3, but also reveal its modulation on p300 HAT activity as the underlying mechanism.


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N.-z. Lei, X.-y. Zhang, H.-z. Chen, Y. Wang, Y.-y. Zhan, Z.-h. Zheng, Y.-m. Shen, and Q. Wu
A feedback regulatory loop between methyltransferase PRMT1 and orphan receptor TR3
Nucleic Acids Res., February 1, 2009; 37(3): 832 - 848.
[Abstract] [Full Text] [PDF]


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