Circadian output genes act downstream of the clock to promote rhythmic changes in behavior and physiology, yet their molecular and cellular functions are not well understood. Here we characterize an interaction between regulators of circadian entrainment, output, and synaptic development in Drosophila that influences clock-driven anticipatory increases in morning and evening activity. We previously showed the JETLAG (JET) E3 ubiquitin ligase resets the clock upon light exposure, whereas the PDZ protein DYSCHRONIC (DYSC) regulates circadian locomotor output and synaptic development. Surprisingly, we find that JET and DYSC antagonistically regulate synaptic development at the larval neuromuscular junction, and reduced JET activity rescues arrhythmicity of dysc mutants. Consistent with our prior finding that DYSC regulates SLOWPOKE (SLO) potassium channel expression, jet mutations also rescue circadian and synaptic phenotypes in slo mutants. Collectively, our data suggest that JET, DYSC, and SLO promote circadian output in part by regulating synaptic morphology.

昼夜节律的输出基因在时钟的下游起作用，以促进行为和生理的节律性变化，但是它们的分子和细胞功能尚不清楚。在这里，我们表征了果蝇昼夜节律，产量和突触发展的监管机构之间的相互作用，影响了时钟驱动的预期的早晨和晚上的活动增加。我们以前的研究表明，JETLAG（JET）E3泛素连接酶在光线照射下会重置时钟，而PDZ蛋白DYSCHRONIC（DYSC）调节昼夜运动能力和突触发育。出人意料的是，我们发现JET和DYSC拮抗幼虫神经肌肉交界处的突触发育，而降低的JET活性可拯救dysc的心律失常突变体。与我们先前发现DYSC调节SLOWPOKE（SLO）钾通道表达的发现一致，jet突变还可以拯救slo突变体中的昼夜节律和突触表型。总体而言，我们的数据表明JET，DYSC和SLO部分通过调节突触形态来促进昼夜节律输出。