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Molecular and Cellular Biology, December 1999, p. 8686-8693, Vol. 19, No. 12
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Disruption of muREC2/RAD51L1 in Mice Results in Early Embryonic Lethality Which Can Be Partially Rescued in a p53minus /minus Background

Zhigang Shu, Sheryl Smith, Lijuan Wang, Michael C. Rice, and Eric B. Kmiec*

Department of Biological Sciences, University of Delaware, Newark, Delaware 19716

Received 12 March 1999/Returned for modification 17 April 1999/Accepted 16 September 1999

muREC2/RAD51L1 is a radiation-inducible gene that regulates cell cycle progression. To elucidate the biological function of muREC2/RAD51L1, the gene was disrupted in embryonic stem cells by homologous recombination. Mice heterozygous for muREC2/RAD51L1 appear normal and fertile; however, no homozygous pups were born after interbreeding of heterozygous mice. Timed pregnancy studies showed that homozygous mutant embryos were severely retarded in growth as early as ca. 5 days gestation (E5.5) and were completely resorbed by E8.5. Mutant blastocyst outgrowth was also severely impaired in a double-knockout embryo, but embryonic development did progress further in a p53-null background. These results suggest that muREC2/RAD51L1 plays a role in cell proliferation and early embryonic development, perhaps through interaction with p53.

* Corresponding author. Mailing address: Department of Biological Sciences, Wolf Hall, University of Delaware, Newark, DE 19716. Phone: (302) 831-3221. Fax: (302) 831-8786. E-mail: ekmiec{at}udel.edu.

Molecular and Cellular Biology, December 1999, p. 8686-8693, Vol. 19, No. 12
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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