The intrinsic ability of individual cells, independent of the master clock in the brain, to maintain an approximate 24-hour rhythm in their gene expression and metabolic activity. This decentralized time keeping, governed by cell-autonomous circadian oscillators, allows peripheral tissues to anticipate and prepare for rhythmic changes in hormonal status and nutrient availability. Disruption of this precise cellular timing is a recognized factor in metabolic and hormonal dysfunction.
Origin
The concept is a subset of chronobiology, moving the focus from the central suprachiasmatic nucleus (SCN) to the peripheral tissues and their self-sustaining clock gene networks. The discovery of the core clock genes established the molecular basis for this cellular rhythmicity. This molecular basis is a recent advancement in our understanding of biology.
Mechanism
The mechanism relies on a transcriptional-translational feedback loop involving key clock proteins like CLOCK, BMAL1, Period (PER), and Cryptochrome (CRY). CLOCK and BMAL1 drive the transcription of PER and CRY, which then inhibit CLOCK/BMAL1 activity, completing the approximately 24-hour cycle. This molecular oscillation is essential for timing the expression of enzymes and receptors that mediate hormonal actions and metabolic processes within the cell.
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