| abstract |
Data presented herein provide a molecular mechanism for circadian gene mPer2 in DNA damage response and tumor suppression in vivo. Mice deficient in mPer2 gene display neoplastic phenotypes. These mice are deficient in p53-mediated apoptosis in thymocytes and have increased tumor occurrences after γ-radiation. Core circadian genes are induced by γ-radiation in wild-type mice but not in mPer2 mutant mice. Temporal expression of genes involved in cell cycle regulation and tumor suppression, such as c-Myc, Cyclin D1, Cyclin A, Mdm-2 and Gadd45α is dependent on mPER2 in vivo. |