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Summary
Phenotypic plasticity, the potential for phenotypic change in response to external signals, drives adaptation to environmental fluctuations and requires flexible gene regulation (1). A seminal example of adaptive plasticity is represented by the circadian clock (2), which establishes 24-hour rhythmicity in physiology, metabolic activities, and behavior. As external time cues, such as light and food intake, can reset the phase of oscillations, circadian homeostasis enables light-sensitive organisms to both anticipate and adapt to daily environmental cycles (2). On page 1274 of this issue, Kim et al. (3) provide a glimpse into the genome-wide complexity of transcriptional plasticity during the physiological circadian cycle in mice, with implications for our understanding of diseases linked with deregulation of the circadian clock (2).
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