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Nucleic Acids Research, 2002, Vol. 30, No. 9 1967-1976
© 2002 Oxford University Press

A single cell cycle genes homology region (CHR) controls cell cycle-dependent transcription of the cdc25C phosphatase gene and is able to cooperate with E2F or Sp1/3 sites

Ulrike Haugwitz, Mark Wasner, Marcus Wiedmann, Katja Spiesbach, Karen Rother, Joachim Mössner and Kurt Engeland*

Department of Internal Medicine II, University of Leipzig, Max Bürger Research Center, Johannisallee 30, D-04103 Leipzig, Germany

The cdc25C phosphatase participates in regulating transition from the G2 phase of the cell cycle to mitosis by dephosphorylating cyclin-dependent kinase 1. The tumor suppressor p53 down-regulates expression of cdc25C as part of G2/M checkpoint control. Transcription of cdc25C oscillates during the cell cycle with no expression in resting cells and maximum transcription in G2. We had identified earlier a new mechanism of cell cycle-dependent transcription that is regulated by a cell cycle-dependent element (CDE) in conjunction with a cell cycle genes homology region (CHR). The human cdc25C gene was the first example. CDE/CHR tandem elements have since been found in promoters of many cell cycle genes. Here we show that the mouse cdc25C gene is regulated by a CHR but does not hold a CDE. Therefore, it is the first identified gene with CHR-dependent transcriptional regulation during the cell cycle not relying on a CDE located upstream of it. The CHR leads to repression of cdc25C transcription early in the cell cycle and directs a release of this repression in G2. Furthermore, we find that this CHR can cooperate in cell cycle-dependent transcription with elements placed directly upstream of it binding E2F, Sp1 or Sp3 transcription factors.

* To whom correspondence should be addressed. Tel: +49 341 9725900; Fax: +49 341 9712209; Email: engeland{at}medizin.uni-leipzig.de


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