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Molecular and Cellular Biology, March 2004, p. 2487-2498, Vol. 24, No. 6
0270-7306/04/$08.00+0     DOI: 10.1128/MCB.24.6.2487-2498.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Cyclin F Disruption Compromises Placental Development and Affects Normal Cell Cycle Execution

Michael T. Tetzlaff,1 Chang Bai,2,{dagger} Milton Finegold,3 John Wilson,2 J. Wade Harper,2,4 Kathleen A. Mahon,5 and Stephen J. Elledge1,2,6,7*

Verna and Marrs McLean Department of Biochemistry,2 Department of Human and Molecular Genetics,1 Howard Hughes Medical Institute,6 Department of Molecular and Cellular Biology,5 Department of Pathology, Texas Children's Hospital, Baylor College of Medicine, Houston, Texas 77030,3 Department of Pathology,4 Department of Genetics and Center for Genetics and Genomics, Harvard Medical School, Boston, Massachusetts 021157

Received 10 October 2003/ Returned for modification 4 November 2003/ Accepted 19 December 2003

Human cyclin F was originally isolated as a cDNA capable of suppressing the temperature sensitivity of a Saccharomyces cerevisiae cdc4-1 mutant. Its tightly regulated expression and high conservation in the evolutionary progression from amphibians to mammals suggest that it coordinates the timing of a critical cell cycle event. The fact that it contains an F box and can form an SCF (Skp1-Cul1/Cdc53-F-box) complex in vivo further suggests that it may also function in proteolysis. To investigate the role of cyclin F in vivo, we generated mice deficient for cyclin F and conditionally deficient mice as well as mouse embryonic fibroblasts (MEFs) conditionally deficient for cyclin F. Heterozygous animals are normal and fertile, but CycF-/- animals, with a myriad of developmental anomalies due in large part to failures in yolk sac and chorioallantoic placentation, die around embryonic day 10.5. Tissue-specific deletion of cyclin F revealed that it was not required for the development and function of a number of different embryonic and adult tissues. In contrast, MEFs lacking cyclin F, while viable, do exhibit cell cycle defects, including reduced population-doubling time and a delay in cell cycle reentry from quiescence, indicating that cyclin F plays a role in cell cycle regulation.

* Corresponding author. Mailing address: Department of Genetics and Center for Genetics and Genomics, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115. Phone: (617) 525-4510. Fax: (617) 525-4500. E-mail: selledge{at}genetics.med.harvard.edu.

{dagger} Present address: Merck Research Laboratories, West Point, Pa.

Molecular and Cellular Biology, March 2004, p. 2487-2498, Vol. 24, No. 6
0022-538X/04/$08.00+0     DOI: 10.1128/MCB.24.6.2487-2498.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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