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Molecular and Cellular Biology, December 2007, p. 8049-8064, Vol. 27, No. 23
0270-7306/07/$08.00+0     doi:10.1128/MCB.00680-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Drosophila DBT Lacking Protein Kinase Activity Produces Long-Period and Arrhythmic Circadian Behavioral and Molecular Rhythms{triangledown} ,{dagger}

Michael J. Muskus,{ddagger} Fabian Preuss,{ddagger},§ Jin-Yuan Fan, Edward S. Bjes, and Jeffrey L. Price*

School of Biological Sciences, Division of Molecular Biology and Biochemistry, University of Missouri-Kansas City, Kansas City, Missouri 64110

Received 18 April 2007/ Returned for modification 25 May 2007/ Accepted 4 September 2007

A mutation (K38R) which specifically eliminates kinase activity was created in the Drosophila melanogaster ckI gene (doubletime [dbt]). In vitro, DBT protein carrying the K38R mutation (DBTK/R) interacted with Period protein (PER) but lacked kinase activity. In cell culture and in flies, DBTK/R antagonized the phosphorylation and degradation of PER, and it damped the oscillation of PER in vivo. Overexpression of short-period, long-period, or wild-type DBT in flies produced the same circadian periods produced by the corresponding alleles of the endogenous gene. These mutations therefore dictate an altered "set point" for period length that is not altered by overexpression. Overexpression of the DBTK/R produced effects proportional to the titration of endogenous DBT, with long circadian periods at lower expression levels and arrhythmicity at higher levels. This first analysis of adult flies with a virtual lack of DBT activity demonstrates that DBT's kinase activity is necessary for normal circadian rhythms and that a general reduction of DBT kinase activity does not produce short periods.

* Corresponding author. Mailing address: School of Biological Sciences, University of Missouri-Kansas City, 5100 Rockhill Rd., Kansas City, MO 64110. Phone: (816) 235-2572. Fax: (816) 235-5595. E-mail: pricejL{at}umkc.edu

{triangledown} Published ahead of print on 24 September 2007.

{dagger} Supplemental material for this article may be found at http://mcb.asm.org/.

{ddagger} M.J.M. and F.P. contributed equally to this study.

§ Present address: Center for Sleep and Circadian Biology, Northwestern University, Evanston, IL 60208.

Molecular and Cellular Biology, December 2007, p. 8049-8064, Vol. 27, No. 23
0270-7306/07/$08.00+0     doi:10.1128/MCB.00680-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

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  • Meissner, R.-A., Kilman, V. L., Lin, J.-M., Allada, R. (2008). TIMELESS Is an Important Mediator of CK2 Effects on Circadian Clock Function In Vivo. J. Neurosci. 28: 9732-9740 [Abstract] [Full Text]  
  • Chiu, J. C., Vanselow, J. T., Kramer, A., Edery, I. (2008). The phospho-occupancy of an atypical SLIMB-binding site on PERIOD that is phosphorylated by DOUBLETIME controls the pace of the clock. Genes Dev. 22: 1758-1772 [Abstract] [Full Text]  


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