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Molecular and Cellular Biology, June 2001, p. 3853-3861, Vol. 21, No. 12
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.12.3853-3861.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Absence of Apparent Phenotype in Mice Lacking Cdc25C Protein Phosphatase

Mei-Shya Chen,1,2 Jonathan Hurov,1 Lynn S. White,1,2 Terry Woodford-Thomas,3 and Helen Piwnica-Worms1,2,*

Department of Cell Biology and Physiology,1 Howard Hughes Medical Institute,2 and Department of Pathology and Immunology,3 Washington University Medical School, St. Louis, Missouri 63110

Received 5 December 2000/Returned for modification 9 January 2001/Accepted 19 March 2001

The Cdc25 family of protein phosphatases positively regulate the cell division cycle by activating cyclin-dependent protein kinases. In humans and rodents, three Cdc25 family members denoted Cdc25A, -B, and -C have been identified. The murine forms of Cdc25 exhibit distinct patterns of expression both during development and in adult mouse tissues. In order to determine unique contributions made by the Cdc25C protein phosphatase to embryonic and adult cell cycles, mice lacking Cdc25C were generated. We report that Cdc25C-/- mice are viable and do not display any obvious abnormalities. Among adult tissues in which Cdc25C is detected, its transcripts are most abundant in testis, followed by thymus, ovary, spleen, and intestine. Mice lacking Cdc25C were fertile, indicating that Cdc25C does not contribute an essential function during spermatogenesis or oogenesis in the mouse. T- and B-cell development was also found to be normal in Cdc25C-/- mice, and Cdc25C-/- mouse splenic T and B cells exhibited normal proliferative responses in vitro. Finally, the phosphorylation status of Cdc2, the timing of entry into mitosis, and the cellular response to DNA damage were unperturbed in mouse embryo fibroblasts lacking Cdc25C. These findings indicate that Cdc25A and/or Cdc25B may compensate for loss of Cdc25C in the mouse.

* Corresponding author. Mailing address: Department of Cell Biology and Physiology & Howard Hughes Medical Institute, Washington University School of Medicine, Box 8228, 660 South Euclid Ave., St. Louis, MO 63110-1093. Phone: (314) 362-6812. Fax: (314) 362-3709. E-mail: hpiwnica{at}cellbio.wustl.edu.

Molecular and Cellular Biology, June 2001, p. 3853-3861, Vol. 21, No. 12
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.12.3853-3861.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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