The review introduces the “arrhythmic zone,” a temperature range in which the internal clock loses its self-sustained rhythm while the cell or organism remains viable
The review introduces the “arrhythmic zone,” a temperature range in which the internal clock loses its self-sustained rhythm while the cell or organism remains viable
On August 24, The FEBS Journal published a review of how cold affects circadian rhythms. The authors compiled evidence from bacteria to mammals and propose distinguishing the temperature at which the clock loses its self-sustained rhythm from the lower temperature limit for viability.
Circadian clocks are intracellular mechanisms that generate a rhythm of approximately one day. Within a certain temperature range, this rhythm remains close to 24 hours even though individual biochemical reactions become faster or slower. This property is called temperature compensation. The review examines what happens below this range, when the rhythm can no longer sustain itself but the cell or organism remains viable.
“We use the term ‘arrhythmic zone’ for the range in which viability is preserved while the self-sustained rhythm weakens or disappears.”
Experiments with cyanobacterial proteins illustrate this pattern well. In a 2017 experiment, researchers mixed three purified proteins, KaiA, KaiB, and KaiC, in a test tube. The resulting system generated circadian oscillations on its own. As the system was cooled toward 19 °C, the rhythmic changes in KaiC became progressively weaker and gradually fell to zero, while the cycle length changed very little. This transition is called a Hopf bifurcation: the amplitude of self-sustained oscillations decays, while their period remains nearly unchanged.
The protein system still responded to external temperature cycles. A cycle close to its intrinsic 24-hour rhythm produced the strongest response. Within the arrhythmic zone, a repeating external signal can therefore impose a rhythm on a mechanism that has lost its self-sustained oscillation.
The review also discusses more complex systems. In thin slices of the mouse suprachiasmatic nucleus, the brain region that sets the rhythm of the whole body, rhythmic changes in calcium levels and gene expression stopped at 15 °C and resumed after warming. In cultured human U2OS cells, viability remained high at 25–37 °C, while the luminescence rhythm of the BMAL1-dLuc genetic reporter, which tracks clock activity, disappeared at approximately 30 °C.
In six participants, hair follicle cells maintained a similar amplitude of clock gene activity after one day at 18 and 28 °C. The authors attributed this result to blood flow, which buffers temperature changes in living tissue. In cell culture, the surrounding medium determines the temperature. In living tissue, blood flow reduces temperature fluctuations.
Researchers can now look for three distinct temperatures in each organism: the lower limit of viability, the limit of self-sustained rhythmicity, and the limit at which an external daily signal can still maintain a rhythm. Psychrophiles, organisms that grow best at 15 °C or below, are especially relevant to this question. Genes of the kaiABC cluster, which are associated with bacterial circadian clocks, have already been found in polar cyanobacteria. The authors propose measuring their self-sustained rhythms at their native temperatures and comparing the three thresholds in organisms adapted to cold.