Failure to proliferate and mitotic arrest of CDK11(p110/p58)-null mutant mice at the blastocyst stage of embryonic cell development.

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