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Molecular and Cellular Biology, April 2006, p. 3124-3134, Vol. 26, No. 8
0270-7306/06/$08.00+0     doi:10.1128/MCB.26.8.3124-3134.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

CtIP Activates Its Own and Cyclin D1 Promoters via the E2F/RB Pathway during G1/S Progression

Feng Liu and Wen-Hwa Lee*

Department of Biological Chemistry, School of Medicine, University of California, Irvine, California 92697

Received 26 October 2005/ Returned for modification 4 December 2005/ Accepted 18 January 2006

Cell cycle progression from G1 to S phase is mainly controlled by E2F transcription factors and RB family proteins. Previously we showed that the presence of CtIP is essential for G1/S transition in primary mouse blastocysts, as well as in NIH 3T3 cells. However, how CtIP executes this function remains to be elucidated. Here we show that in NIH 3T3 cells the expression of CtIP is regulated by the E2F/RB pathway during late G1 and S phases. The presence of wild-type CtIP, but not the E157K mutant form, which failed to interact with RB, enhanced its own promoter activity. Chromatin immunoprecipitation analysis indicated that the recruitment of CtIP to its promoter occurs concomitantly with TFIIB, a component of the RNA polymerase II complex, and with dissociation of RB from the promoter during late G1 and G1/S transition. Similar positive regulation of cyclin D1 expression by CtIP was also observed. Consistently, cells expressing the CtIP(E157K) protein alone exhibited growth retardation, an increase in the G1 population, and a decrease in the S-phase population. Taken together, these results suggest that, contrary to the postulated universal corepressor role, CtIP activates a subset of E2F-responsive promoters by releasing RB-imposed repression and therefore promotes G1/S progression.

* Corresponding author. Mailing address: Department of Biological Chemistry, 839 Medical Science Court, 124 Sprague Hall, University of California, Irvine, CA 92697. Phone: (949) 824-4492. Fax: (949) 824-9767. E-mail: whlee{at}uci.edu.

Molecular and Cellular Biology, April 2006, p. 3124-3134, Vol. 26, No. 8
0270-7306/06/$08.00+0     doi:10.1128/MCB.26.8.3124-3134.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Huertas, P., Jackson, S. P. (2009). Human CtIP Mediates Cell Cycle Control of DNA End Resection and Double Strand Break Repair. J. Biol. Chem. 284: 9558-9565 [Abstract] [Full Text]  
  • Wu, M., Soler, D. R., Abba, M. C., Nunez, M. I., Baer, R., Hatzis, C., Llombart-Cussac, A., Llombart-Bosch, A., Aldaz, C. M. (2007). CtIP Silencing as a Novel Mechanism of Tamoxifen Resistance in Breast Cancer. Mol Cancer Res 5: 1285-1295 [Abstract] [Full Text]  


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