The mammalian circadian oscillator is composed of interacting positive and 
negative transcription events. The clock proteins PER1 and PER2 play essential 
roles in a negative limb of the feedback loop that generates the circadian 
rhythm in mammals. In addition, the proteins CLOCK and BMAL1 (also known as 
ARNTL) form a heterodimer that drives the Per genes via the E-box consensus 
sequences within their promoter regions. In the present study, we demonstrate 
that Id2 is involved in stabilization of the amplitudes of the circadian 
oscillations by suppressing transcriptional activation of clock genes Clock and 
Bmal1. Id2 shows dynamic oscillation in the SCN, with a peak in the late 
subjective night. Under constant dark conditions (DD), Id2(-/-) mice showed no 
apparent difference in locomotor activity, however, under constant light 
conditions (LL), Id2(-/-) mice exhibit aberrant locomotor activity, with lower 
circadian oscillation amplitudes, although the free running periods in Id2(-/-) 
mice show no differences from those in either wild type or heterozygous mice. 
Id2(-/-) animals also exhibit upregulation of Per1 in constant light, during 
both the subjective night and day. In wild type mice, Id2 is upregulated by 
constant light exposure during the subjective night. We propose that Id2 
expression in the SCN contributes to maintenance of dynamic circadian 
oscillations.