Leloup J C, Goldbeter A
Unité de Chronobiologie théorique, Faculté des Sciences, Université Libre de Bruxelles, Campus Plaine, C.P. 231, B-1050 Brussels, Belgium.
Am J Physiol Regul Integr Comp Physiol. 2001 Apr;280(4):R1206-12. doi: 10.1152/ajpregu.2001.280.4.R1206.
With the use of a molecular model for circadian rhythms in Drosophila based on transcriptional regulation, we show how a single, critical pulse of light can permanently suppress circadian rhythmicity, whereas a second light pulse can restore the abolished rhythm. The phenomena occur via the pulsatile induction of either protein degradation or gene expression in conditions in which a stable steady state coexists with stable circadian oscillations of the limit cycle type. The model indicates that suppression by a light pulse can only be accounted for by assuming that the biochemical effects of such a pulse much outlast its actual duration. We determine the characteristics of critical pulses suppressing the oscillations as a function of the phase at which the rhythm is perturbed. The model predicts how the amplitude and duration of the biochemical changes induced by critical pulses vary with this phase. The results provide a molecular, dynamic explanation for the long-term suppression of circadian rhythms observed in a variety of organisms in response to a single light pulse and for the subsequent restoration of the rhythms by a second light pulse.
利用基于转录调控的果蝇昼夜节律分子模型，我们展示了单个关键光脉冲如何能永久抑制昼夜节律性，而第二个光脉冲又如何能恢复被消除的节律。这些现象通过在稳定稳态与极限环型稳定昼夜振荡共存的条件下，蛋白质降解或基因表达的脉冲诱导而发生。该模型表明，光脉冲的抑制作用只能通过假设这种脉冲的生化效应比其实际持续时间长得多来解释。我们确定了抑制振荡的关键脉冲的特征，它是被扰动节律相位的函数。该模型预测了关键脉冲诱导的生化变化的幅度和持续时间如何随此相位而变化。这些结果为在多种生物体中观察到的对单个光脉冲响应时昼夜节律的长期抑制以及随后第二个光脉冲使节律恢复提供了分子动力学解释。
