Nucleic Acids Research Advance Access originally published online on November 10, 2006
Nucleic Acids Research 2006 34(21):6272-6285; doi:10.1093/nar/gkl801
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Nucleic Acids Research, 2006, Vol. 34, No. 21 6272-6285
© 2006 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-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Molecular Biology |
Inhibition of CBF/NF-Y mediated transcription activation arrests cells at G2/M phase and suppresses expression of genes activated at G2/M phase of the cell cycle
1 Department of Molecular Genetics Houston, TX 77030, USA 2 Department of Molecular Pathology, The University of Texas M. D. Anderson Cancer center Houston, TX 77030, USA 3 Genes and Development program, The University of Texas, Graduate School of Biomedical Sciences Houston, TX 77030, USA
*To whom correspondence should be addressed. Tel: +1 713 834 6369; Fax: +1 713 834 6318; Email: smaity{at}mdanderson.org
Received September 8, 2006. Accepted September 28, 2006.
Previous studies showed that binding of the CBF/NF-Y (CBF) transcription factor to cellular promoters is essential for cell proliferation. This observation prompted us to investigate the function of CBF in relation to cell cycle progression and in cell-cycle-regulated transcription. In this study, we used a tetracycline-inducible adenoviral vector to express a truncated CBF-B subunit, Bdbd, lacking a transcription activation domain in various mammalian cell lines. The Bdbd polypeptide interacts with cellular CBF-A/CBF-C and binds to promoters containing CBF-binding sites. Interestingly, expression of Bdbd in various mammalian cells resulted in the inhibition of cell proliferation and specific cell cycle arrest at G2/M phase. Gene expression analysis demonstrated that the expression of Bdbd strongly suppressed cell cycle-dependent transcription activation of Cyclin B1, Aurora A and CDK1 genes, key regulators for cell cycle progression at G2/M phase. Chromatin immunoprecipitation analysis showed that Bdbd significantly inhibited binding of TATA-binding protein, TBP to both Cyclin B1 and Aurora A promoters, but did not inhibit binding of E2F3 activator to Cyclin B1 promoter. This study suggested that the activation domain of CBF-B plays an essential role in the transcription activation of Cyclin B1 and Aurora A genes at G2/M phase, thus regulating cell cycle progression at G2/M phase.
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