ID2 is a rhythmically expressed helix–loop–helix transcriptional repressor, and its deletion results in abnormal properties of photoentrainment. By examining parametric and nonparametric models of entrainment, we have started to explore the mechanism underlying this circadian phenotype. Id2-/- mice were exposed to differing photoperiods, and the phase angle of entrainment under short days was delayed 2 h as compared with controls. When exposed to long durations of continuous light, enhanced entrainment responses were observed after a delay of the clock but not with phase advances. However, the magnitude of phase shifts was not different in Id2-/- mice tested in constant darkness using a discrete pulse of saturating light. No differences were observed in the speed of clock resetting when challenged by a series of discrete pulses interspaced by varying time intervals. A photic phase-response curve was constructed, although no genotypic differences were observed. Although phase shifts produced by discrete saturating light pulses at CT16 were similar, treatment with a subsaturating pulse revealed a ~2-fold increase in the magnitude of the Id2-/- shift. A corresponding elevation of light-induced per1 expression was observed in the Id2-/- suprachiasmatic nucleus (SCN). To test whether the phenotype is based on a sensitivity change at the level of the retina, pupil constriction responses were measured. No differences were observed in responses or in retinal histology, suggesting that the phenotype occurs downstream of the retina and retinal hypothalamic tract. To test whether the phenotype is due to a reduced amplitude of state variables of the clock, the expression of clock genes per1 and per2 was assessed in vivo and in SCN tissue explants. Amplitude, phase, and period length were normal in Id2-/- mice. These findings suggest that ID2 contributes to a photoregulatory mechanism at the level of the SCN central pacemaker through control of the photic induction of negative elements of the clock.

ID2 是一种有节奏地表达的螺旋-环-螺旋转录抑制因子，其缺失会导致光夹带的异常特性。通过检查夹带的参数和非参数模型，我们已经开始探索这种昼夜节律表型的机制。Id2 -/- 小鼠暴露于不同的光周期，与对照组相比，短日夹带的相位角延迟了2小时。当暴露在长时间的连续光下时，在时钟延迟后观察到增强的夹带响应，但没有相位提前。然而， Id2中的相移幅度并无不同-/- 小鼠在持续黑暗中使用饱和光的离散脉冲进行测试。当受到一系列由不同时间间隔隔开的离散脉冲的挑战时，时钟重置的速度没有观察到差异。尽管没有观察到基因型差异，但构建了光相响应曲线。尽管 CT16 处离散饱和光脉冲产生的相移相似，但用次饱和脉冲处理显示Id2 -/- 偏移幅度增加了约 2 倍。在Id2中观察到光诱导per1表达的相应升高-/- 视交叉上核 (SCN)。为了测试表型是否基于视网膜水平的敏感性变化，测量了瞳孔收缩反应。在反应或视网膜组织学中未观察到差异，表明表型发生在视网膜和视网膜下丘脑束的下游。为了测试表型是否是由于时钟状态变量幅度的降低，在体内和 SCN 组织外植体中评估了时钟基因per1和per2的表达。Id2中幅度、相位和周期长度正常-/- 老鼠。这些发现表明，ID2 通过控制时钟负元素的光感应，有助于 SCN 中央起搏器水平的光调节机制。