Redondance génétique et synchronisation cellulaire dans les horloges circadiennes

Complex interactions in circadian timing may allow for genetic redundancy in the absence of the CLOCK gene.

• Circadian clocks in mammals rely on a network of feedback loops and various molecular processes.
• The CLOCK/BMAL1 heterodimer is a key component in maintaining circadian rhythms.
• Data from Clock knock-out mice indicate that the Npas2 gene can compensate for the loss of CLOCK.
• Persistent rhythmicity in the suprachiasmatic nuclei may result from genetic redundancy and strong intercellular connections.
• These intercellular connections appear to be weaker in peripheral tissues such as the liver and lung.

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