dyschronic, a Drosophila Homolog of a Deaf-Blindness Gene, Regulates Circadian Output and Slowpoke Channels

• DOI: 10.1371/journal.pgen.1002671
• Publication Date: 2012-04-19T20:52:06Z
• Authors: James E. C. Jepson; Mohammad Shahidullah; Angelique Lamaze; Drew Peterson; Huihui Pan; Kyunghee Koh
• Keywords: Genetic screen; Timeless

Many aspects of behavior and physiology are under circadian control. In Drosophila, the molecular clock that regulates rhythmic patterns has been extensively characterized. contrast, genetic loci involved in linking to alterations motor activity have remained elusive. a forward-genetic screen, we uncovered new component output pathway, which termed dyschronic (dysc). dysc mutants exhibit arrhythmic locomotor behavior, yet their eclosion rhythms normal protein cycling remains intact. Intriguingly, is closest Drosophila homolog whirlin, gene linked type II Usher syndrome, leading cause deaf-blindness humans. Whirlin other proteins expressed mammalian central nervous system, function CNS not investigated. We show DYSC major neuronal tracts expression calcium-activated potassium channel SLOWPOKE (SLO), an ion also required pathway. SLO co-localized brain control each other's post-transcriptionally. Co-immunoprecipitation experiments demonstrate they form complex, suggesting regulate through protein–protein interaction. Furthermore, electrophysiological recordings neurons adult SLO-dependent currents greatly reduced mutants. Our work identifies as pathway important regulator expression, suggests novel roles for system.