In mammals, circadian rhythms in behavior and physiology are controlled by a 
central pacemaker, the SCN, and subordinated clocks throughout the body. On the 
molecular level, these clocks are based on transcriptional/translational 
feedback loops involving a set of clock genes that regulate their own 
transcription. Among the components driving the mammalian circadian clock are 
the Period 1 and 2 (Per1 and Per2) and Cryptochrome 1 and 2 (Cry1 and Cry2) 
genes. In the present study, the authors characterize the behavioral and 
molecular rhythms of Per2/Cry1 double mutant mice under 3 different lighting 
conditions. In an LD cycle, the activity of these animals is masked by light, 
while in DD, the mutants lose circadian rhythmicity but exhibit strong ultradian 
rhythms. In LL of higher intensity, circadian rhythms are restored on the 
behavioral level with a drastically shortened endogenous period. Furthermore, 
both in the SCN and in the periphery, clock gene rhythms are restored. Based on 
these observations and also on the fact that light-mediated induction of Per 
gene expression is preserved in these mutants, the authors propose a mechanism 
by which endogenous ultradian rhythms may relay timed light exposure to the SCN, 
leading to a reinitiation of self-sustained circadian rhythms in LL.