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Mice lacking cyclin D1 are small and show defects in eye and mammary gland development.

Genes & development | Oct 1, 1995

Using homologous recombination, mice lacking cyclin D1 were generated by replacing most of the first exon of the Cyl-1 gene with sequences encoding neomycin resistance. Cyl-1(-1-) mice were viable and fertile but consistently smaller than their heterozygous or wild-type littermates. The nullizygous animals also showed two distinctive abnormalities: a severe retinopathy caused by impaired development of all layers of the retina and, in the mammary gland during pregnancy, a marked reduction in acinar development accompanied by a failure to lactate. Approximately 50% of animals also had a malformation of the jaw that manifested itself as a misalignment of the incisor teeth. Mouse embryo fibroblasts isolated from 14 day nullizygous, heterozygous, or wild-type embryos and grown under standard conditions showed similar cell-cycle and growth characteristics. Thus although cyclin D1 kinase activity may facilitate G1 progression, it is not essential for the development of most tissues and organs, and only a few specialized cell lineages are demonstrably sensitive to its absence.

Pubmed ID: 7557388 RIS Download

Mesh terms: Animals | Base Sequence | Body Constitution | Cell Cycle | Cell Differentiation | Cells, Cultured | Cyclin D1 | Cyclins | DNA Primers | Female | Fibroblasts | Gene Expression | Gene Targeting | Heterozygote | Homozygote | Jaw Abnormalities | Mammary Glands, Animal | Mice | Mice, Transgenic | Molecular Sequence Data | Oncogene Proteins | Pregnancy | Recombination, Genetic | Retina | Stem Cells

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Mouse Genome Informatics (Data, Gene Annotation)

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