We have been using proteomic and genetic approaches to identify proteins and cellular pathways that interact with DBT, the principal kinase targeting circadian transcription factor PER for phosphorylation and degradation.The proteomic approach identified a previously unstudied protein that interacts with DBT.RNAi-mediated knock-down of its mRNA produced behavioral arrhythmicity, high levels of hypophosphorylated nuclear PER and altered DBT.