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A clock shock: mouse CLOCK is not required for circadian oscillator function.

Jason P Debruyne¹, Elizabeth Noton, Christopher M Lambert

¹Department of Neurobiology, University of Massachusetts Medical School, 364 Plantation Street, Worcester, Massachusetts 01605, USA.

|May 6, 2006

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CLOCK-deficient mice still exhibit circadian rhythms, challenging the necessity of CLOCK:BMAL1 heterodimers for mammalian clock function. These findings impact our understanding of the core circadian clock mechanism.

Area of Science:

Chronobiology
Molecular Biology
Genetics

Background:

The mammalian circadian clock relies on transcriptional feedback loops.
CLOCK and BMAL1 are considered essential transcription factors for circadian rhythmicity.

Purpose of the Study:

To investigate the role of CLOCK in the circadian clock mechanism.
To evaluate the circadian phenotypes of CLOCK-deficient mice.

Main Methods:

Generation of whole-animal CLOCK knockouts using the Cre-LoxP system.
Assessment of circadian phenotypes, including locomotor activity and light responses.
Analysis of clock gene mRNA and protein levels in the suprachiasmatic nuclei and liver.

Main Results:

Related Experiment Videos

CLOCK-deficient mice maintain robust circadian rhythms in locomotor activity.

Altered responses to light were observed in CLOCK-deficient mice.

Molecular feedback loops in the circadian clock continue to function despite CLOCK deficiency, with altered gene expression.

Conclusions:

The necessity of CLOCK:BMAL1 heterodimers for circadian clock function is challenged.
CLOCK is not strictly essential for maintaining robust circadian rhythms in mice.
The study provides new insights into the flexibility and redundancy within the mammalian circadian clock system.