A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Reference Report

Reference
Citation Martinek, S., Inonog, S., Manoukian, A.S., Young, M.W. (2001). A role for the segment polarity gene shaggy/GSK-3 in the Drosophila circadian clock.  Cell 105(6): 769--779. (Export to RIS)
FlyBase ID FBrf0136819
Publication Type Research paper
PubMed ID 11440719
PubMed Abstract Tissue-specific overexpression of the glycogen synthase kinase-3 (GSK-3) ortholog shaggy (sgg) shortens the period of the Drosophila circadian locomotor activity cycle. The short period phenotype was attributed to premature nuclear translocation of the PERIOD/TIMELESS heterodimer. Reducing SGG/GSK-3 activity lengthens period, demonstrating an intrinsic role for the kinase in circadian rhythmicity. Lowered sgg activity decreased TIMELESS phosphorylation, and it was found that GSK-3 beta specifically phosphorylates TIMELESS in vitro. Overexpression of sgg in vivo converts hypophosphorylated TIMELESS to a hyperphosphorylated protein whose electrophoretic mobility, and light and phosphatase sensitivity, are indistinguishable from the rhythmically produced hyperphosphorylated TIMELESS of wild-type flies. Our results indicate a role for SGG/GSK-3 in TIMELESS phosphorylation and in the regulated nuclear translocation of the PERIOD/TIMELESS heterodimer.
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Language of Publication English
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Publication Type Journal
Abbreviation Cell
Title Cell
Publication Year 1974-
ISBN/ISSN 0092-8674
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