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Nucleic Acids Research 2004 32(11):3462-3468; doi:10.1093/nar/gkh669
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Published online 29 June 2004

Nucleic Acids Research, Vol. 32 No. 11 © Oxford University Press 2004; all rights reserved

Promoter-binding and repression of PDGFRB by c-Myc are separable activities

Daniel Y. L. Mao1,2, Dalia Barsyte-Lovejoy2, Cynthia S. W. Ho1,2, John D. Watson2, Angelina Stojanova1,2 and Linda Z. Penn1,2,*

1 Department of Medical Biophysics, University of Toronto and 2 Department of Cellular and Molecular Biology, Ontario Cancer Institute/Princess Margaret Hospital, 610 University Avenue, Toronto, Ontario M5G 2M9, Canada

* To whom correspondence should be addressed at OCI/PMH, 610 University Avenue, Toronto, Ontario M5S 2M9, Canada. Tel: +1 416 946 2276; Fax: +1 416 946 2840; Email: lpenn{at}uhnres.utoronto.ca
Present address: Cynthia S. W. Ho, Samuel Lunenfeld Research Institute/Mount Sinai Hospital, 600 University Avenue, Toronto, Ontario M5G 1X5, Canada

Received April 4, 2004; Revised and Accepted June 7, 2004

The c-Myc transcription factor represses the mRNA expression of the platelet-derived growth factor receptor beta gene (PDGFRB). Using chromatin immunoprecipitation, we show that c-Myc binds to the proximal promoter of the PDGFRB gene in proliferating rat fibroblasts. Interestingly, mutant c-Myc proteins that are unable to repress PDGFRB gene expression, c-MycdBR and c-Mycd106-143, are still able to bind to the promoter in vivo. Hence, promoter-binding and repression of PDGFRB by c-Myc are separable activities. We also show that Myc repression of PDGFRB is not dependent on previously described or known transactivator-binding regions, suggesting Myc may be recruited to the promoter by multiple or yet unidentified transcription factors. In the presence of intact promoter-binding by Myc, trichostatin A (TSA) can block Myc repression of PDGFRB in vivo, again demonstrating that promoter-binding and repression are separable. Taken together, we hypothesize that Myc repression of PDGFRB expression occurs by a multi-step mechanism in which repression is initiated after Myc is recruited to the promoter.


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