Open AccessMice thrive without Cdk4 and Cdk2
Author(s) -
Barrière Cédric,
Santamaría David,
Cerqueira Antonio,
Galán Javier,
Martín Alberto,
Ortega Sagrario,
Malumbres Marcos,
Dubus Pierre,
Barbacid Mariano
Publication year - 2007
Publication title -
molecular oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.332
H-Index - 88
eISSN - 1878-0261
pISSN - 1574-7891
DOI - 10.1016/j.molonc.2007.03.001
Subject(s) - cyclin dependent kinase 6 , cyclin dependent kinase 2 , cyclin dependent kinase , microbiology and biotechnology , cyclin dependent kinase 1 , biology , cell cycle , kinase , cell , biochemistry , protein kinase a
Mammalian cell division is thought to be driven by sequential activation of several Cyclin‐dependent kinases (Cdk), mainly Cdk4, Cdk6, Cdk2 and Cdk1. Since mice lacking Cdk4, Cdk6 or Cdk2 are viable, it has been proposed that they play compensatory roles. We report here that mice lacking Cdk4 and Cdk2 complete embryonic development to die shortly thereafter presumably due to heart failure. However, conditional ablation of Cdk2 in adult mice lacking Cdk4 does not result in obvious abnormalities. Moreover, these double mutant mice recover normally after partial hepatectomy. In culture, Cdk4−/−;Cdk2−/−embryonic fibroblasts become immortal, display robust pRb phosphorylation and have normal S phase kinetics. These observations indicate that Cdk4 and Cdk2 are dispensable for the mammalian cell cycle and for adult homeostasis.