Katherina Martinez, Andy LiWang
Circadian clocks are endogenous oscillators that coordinate physiology and behavior with the 24-h day-night cycle. Temperature compensation-the maintenance of a near-constant period across a range of temperatures-is a hallmark of circadian systems, but it has a lower bound. In diverse organisms, circadian rhythms can weaken or disappear at temperatures that remain within the organism's broader physiological survival range. We refer to this interval, where viability is retained but autonomous rhythmicity is diminished or lost, as the "arrhythmic zone" (AZ): the temperature range bounded above by the lower critical temperature for circadian rhythmicity and below by the organism's minimum viable temperature. Evidence for such low-temperature clock failure has been reported in cyanobacteria, plants, fungi, insects, marine invertebrates, and mammals, although the strength and mechanistic resolution of that evidence vary across systems. In cyanobacteria, low-temperature clock failure occurs through Hopf bifurcation at ~ 19°C, whereas in Arabidopsis rhythmic clock gene expression is strongly damped or disrupted at 4°C, and in hibernating mammalian SCN tissue molecular rhythms arrest below ~ 15-17°C, all at temperatures within the organism's broader survival range. This review synthesizes evidence for low-temperature limits of circadian function across model systems, examines candidate mechanisms of clock failure, evaluates hypotheses for possible adaptive significance, and highlights the near-complete absence of circadian data from true psychrophiles.