Chunghun Lim1*, Jongbin Lee2*, Changtaek Choi2, Valerie L. Kilman1, Juwon Kim2, Sung Mi Park3, Sung Key Jang3, Ravi Allada1& Joonho Choe2
1Department of Neurobiology and Physiology, Northwestern University, Evanston, Illinois 60208, USA. 2Department of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon 305-701, Korea. 3Department of Life Sciences, Pohang University of Science and Technology, Pohang 790-784, Korea.
*These authors contributed equally to this work
Daily oscillations of gene expression underlie circadian behaviours in multicellular organisms1. While attention has been focused on transcriptional and post-translational mechanisms1-3, other posttranscriptional modes have been less clearly delineated. Here we report mutants of a novel Drosophila gene twenty-four (tyf) that show weak behavioural rhythms. Weak rhythms are accompanied by marked reductions in the levels of the clock protein Period (PER) as well as more modest effects on Timeless (TIM). Nonetheless, PER induction in pacemaker neurons can rescue tyf mutant rhythms. TYF associates with a 5'-cap-binding complex, poly(A)-binding protein (PABP), as well as per andtim transcripts. Furthermore, TYF activates reporter expression when tethered to reporter messenger RNA even in vitro. Taken together, these data indicate that TYF potently activates PER translation in pacemaker neurons to sustain robust rhythms, revealing a new and important role for translational control in the Drosophila circadian clock.