Abstract
Daily oscillations of gene expression underlie circadian behaviours in multicellular organisms1. While attention has been focused on transcriptional and posttranslational mechanisms1–3, other posttranscriptional modes have been less clearly delineated. Here we report mutants of a novel Drosophila gene twenty-four (tyf) that display weak behavioural rhythms. Weak rhythms are accompanied by dramatic 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 and tim transcripts. Furthermore, TYF activates reporter expression when tethered to reporter mRNA even in vitro. Taken together, these data suggest that TYF potently activates PER translation in pacemaker neurons to sustain robust rhythms, revealing a novel and important role for translational control in the Drosophila circadian clock.
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