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Molecular and Cellular Biology, April 2004, p. 3188-3197, Vol. 24, No. 8
0270-7306/04/$08.00+0     DOI: 10.1128/MCB.24.8.3188-3197.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Failure To Proliferate and Mitotic Arrest of CDK11p110/p58-Null Mutant Mice at the Blastocyst Stage of Embryonic Cell Development

Tongyuan Li,1,2 Akira Inoue,1 Jill M. Lahti,1 and Vincent J. Kidd1,2*

Department of Genetics and Tumor Cell Biology, St. Jude Children's Research Hospital,1 Department of Molecular Sciences, School of Medicine, University of Tennessee Health Science Center, Memphis, Tennessee 381052

Received 23 October 2003/ Returned for modification 15 December 2003/ Accepted 15 January 2004

The CDK11p110 protein kinases are part of large-molecular-weight complexes that also contain RNA polymerase II, transcriptional elongation factors, and general pre-mRNA splicing factors. CDK11p110 isoforms may therefore couple transcription and pre-mRNA splicing by their effect(s) on certain proteins required for these processes. The CDK11p58 kinase isoform is generated from the CDK11p110 mRNA through the use of an internal ribosome entry site in a mitosis-specific manner, suggesting that this kinase may regulate the cell cycle during mitosis. The in vivo role and necessity of CDK11p110/p58 kinase function during mammalian development were examined by generating CDK11p110/p58-null mice through targeted disruption of the corresponding gene using homologous recombination. While heterozygous mice develop normally, disruption of both CDK11p110/p58 alleles results in early embryonic lethality due to apoptosis of the blastocyst cells between 3.5 and 4 days postcoitus. Cells within these embryos exhibit both proliferative defect(s) and a mitotic arrest. These results are consistent with the proposed cellular functions of the CDK11p110/p58 kinases and confirm that the CDK11p110/p58 kinases are essential for cellular viability as well as normal early embryonic development.

* Corresponding author. Mailing address: Department of Genetics and Tumor Cell Biology, St. Jude Children's Research Hospital, 332 N. Lauderdale, Memphis, TN 38105. Phone: (901) 495-3469. Fax: (901) 495-2381. E-mail: vincent.kidd{at}stjude.org.

Molecular and Cellular Biology, April 2004, p. 3188-3197, Vol. 24, No. 8
0022-538X/04/$08.00+0     DOI: 10.1128/MCB.24.8.3188-3197.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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