It has been reported that disruption of the circadian clock may lead to 
increased risk of breast cancer in humans and to a high rate or ionizing 
radiation-induced tumors and mortality in mice. Cryptochrome 1 and cryptochrome 
2 proteins are core components of the mammalian circadian clock and mice mutated 
in both genes are arrhythmic. We tested Cry1-/- Cry2-/- mice and fibroblasts 
derived from these mice for radiation-induced cancer and killing and DNA damage 
checkpoints and killing, respectively. We find that the mutant mice are 
indistinguishable from the wild-type controls with respect to radiation-induced 
morbidity and mortality. Similarly, the Cry1-/- Cry2-/-mutant fibroblasts are 
indistinguishable from the wild-type controls with respect to their sensitivity 
to ionizing radiation and UV radiation and ionizing radiation-induced DNA damage 
checkpoint response. Our data suggest that disruption of the circadian clock in 
itself does not compromise mammalian DNA repair and DNA damage checkpoints and 
does not predispose mice to spontaneous and ionizing radiation-induced cancers. 
We conclude that the effect of circadian clock disruption on cellular response 
to DNA damage and cancer predisposition in mice may depend on the mechanism by 
which the clock is disrupted.