| First Author | Fantl V | Year | 1995 |
| Journal | Genes Dev | Volume | 9 |
| Issue | 19 | Pages | 2364-72 |
| PubMed ID | 7557388 | Mgi Jnum | J:29258 |
| Mgi Id | MGI:76789 | Doi | 10.1101/gad.9.19.2364 |
| Citation | Fantl V, et al. (1995) Mice lacking cyclin D1 are small and show defects in eye and mammary gland development. Genes Dev 9(19):2364-72 |
| abstractText | 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. |
