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Cell. 2001 Jun 15;105(6):769-79.

A role for the segment polarity gene shaggy/GSK-3 in the Drosophila circadian clock.

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1
Laboratory of Genetics and National Science Foundation Science and Technology Center for Biological Timing, The Rockefeller University, New York, NY 10021, USA.

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.

PMID:
11440719
DOI:
10.1016/s0092-8674(01)00383-x
[Indexed for MEDLINE]
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