Restoration of Circadian Rhythmicity in Circadian Clock-Deficient Mice in Constant Light

May 30, 2006Journal of biological rhythms

Restoring daily body clock rhythms in mice lacking a circadian clock under constant light

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Abstract

In the presence of high-intensity light, circadian rhythms are restored in Per2/Cry1 double mutant mice.

Under a light/dark cycle, Per2/Cry1 double mutant mice show activity masked by light.
In constant darkness, these mutants lose circadian rhythmicity but display strong ultradian rhythms.
Exposure to high-intensity light results in a significantly shortened endogenous period and restoration of behavioral circadian rhythms.
Clock gene rhythms in both the SCN and peripheral tissues are also restored under high-intensity light conditions.
Light exposure continues to induce expression of Per genes in the mutants, suggesting a potential mechanism for reestablishing circadian rhythms.

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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.

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Restoration of Circadian Rhythmicity in Circadian Clock-Deficient Mice in Constant Light

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