Abstract

BDBT interacts with the circadian kinase DBT and accumulates in eye foci during the dark of a light:dark cycle. BDBT is shown here to be constitutively high in the dark and constitutively low in the light. Analysis of circadian photoreceptor cry and visual photoreceptor ninaE mutants showed that disappearance of eye BDBT foci depends upon both the CRY and the RHODOPSIN-1 pathways. The Arr1 and Arr2 mutants which affect rhodopsin quenching eliminated the accumulation of BDBT foci under dark conditions.Arr1 and Arr2 mutants also lead to increased nuclear accumulation of PER protein. Knock-down of BDBT specifically in the eye produced a loss of coupled circadian localization oscillations for both PER and DBT. PER was constitutively nuclear and DBT was constitutively cytosolic. The results show that BDBT is necessary for co-transport of DBT and PER into the nucleus and suggest that this process is regulated by a light dependent mechanism.

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