A molecular explanation for the long-term suppression of circadian rhythmsby a single light pulse

With the use of a molecular model for circadian rhythms in Drosophila based on transcriptional regulation, we show how a single, critical pulse of lig ht can permanently suppress circadian rhythmicity, whereas a second light p ulse can restore the abolished rhythm. The phenomena occur via the pulsatil e 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 pu lse can only be accounted for by assuming that the biochemical effects of s uch a pulse much outlast its actual duration. We determine the characterist ics of critical pulses suppressing the oscillations as a function of the ph ase at which the rhythm is perturbed. The model predicts how the amplitude and duration of the biochemical changes induced by critical pulses vary wit h this phase. The results provide a molecular, dynamic explanation for the long-term suppression of circadian rhythms observed in a variety of organis ms in response to a single light pulse and for the subsequent restoration o f the rhythms by a second light pulse.