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Genetics
2009 Jan 01;1811:139-52. doi: 10.1534/genetics.108.094805.
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Drosophila and vertebrate casein kinase Idelta exhibits evolutionary conservation of circadian function.
Fan JY
,
Preuss F
,
Muskus MJ
,
Bjes ES
,
Price JL
.
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Mutations lowering the kinase activity of Drosophila Doubletime (DBT) and vertebrate casein kinase Iepsilon/delta (CKIepsilon/delta) produce long-period, short-period, and arrhythmic circadian rhythms. Since most ckI short-period mutants have been isolated in mammals, while the long-period mutants have been found mostly in Drosophila, lowered kinase activity may have opposite consequences in flies and vertebrates, because of differences between the kinases or their circadian mechanisms. However, the results of this article establish that the Drosophila dbt mutations have similar effects on period (PER) protein phosphorylation by the fly and vertebrate enzymes in vitro and that Drosophila DBT has an inhibitory C-terminal domain and exhibits autophosphorylation, as does vertebrate CKIepsilon/delta. Moreover, expression of either Drosophila DBT or the vertebrate CKIdelta kinase carrying the Drosophila dbt(S) or vertebrate tau mutations in all circadian cells leads to short-period circadian rhythms. By contrast, vertebrate CKIdelta carrying the dbt(L) mutation does not lengthen circadian rhythms, while Drosophila DBT(L) does. Different effects of the dbt(S) and tau mutations on the oscillations of PER phosphorylation suggest that the mutations shorten the circadian period differently. The results demonstrate a high degree of evolutionary conservation of fly and vertebrate CKIdelta and of the functions affected by their period-shortening mutations.
Bao,
The Drosophila double-timeS mutation delays the nuclear accumulation of period protein and affects the feedback regulation of period mRNA.
2001, Pubmed
Bao,
The Drosophila double-timeS mutation delays the nuclear accumulation of period protein and affects the feedback regulation of period mRNA.
2001,
Pubmed
Cegielska,
Autoinhibition of casein kinase I epsilon (CKI epsilon) is relieved by protein phosphatases and limited proteolysis.
1998,
Pubmed
Chiu,
The phospho-occupancy of an atypical SLIMB-binding site on PERIOD that is phosphorylated by DOUBLETIME controls the pace of the clock.
2008,
Pubmed
Constance,
The circadian clock-containing photoreceptor cells in Xenopus laevis express several isoforms of casein kinase I.
2005,
Pubmed
,
Xenbase
Cyran,
The double-time protein kinase regulates the subcellular localization of the Drosophila clock protein period.
2005,
Pubmed
Edery,
Temporal phosphorylation of the Drosophila period protein.
1994,
Pubmed
Eide,
The circadian regulatory proteins BMAL1 and cryptochromes are substrates of casein kinase Iepsilon.
2002,
Pubmed
Eide,
Control of mammalian circadian rhythm by CKIepsilon-regulated proteasome-mediated PER2 degradation.
2005,
Pubmed
Fang,
Post-translational regulation of the Drosophila circadian clock requires protein phosphatase 1 (PP1).
2007,
Pubmed
Gallego,
An opposite role for tau in circadian rhythms revealed by mathematical modeling.
2006,
Pubmed
Gallego,
Protein phosphatase 1 regulates the stability of the circadian protein PER2.
2006,
Pubmed
,
Xenbase
Garceau,
Alternative initiation of translation and time-specific phosphorylation yield multiple forms of the essential clock protein FREQUENCY.
1997,
Pubmed
Graves,
Role of COOH-terminal phosphorylation in the regulation of casein kinase I delta.
1995,
Pubmed
Harms,
Posttranscriptional and posttranslational regulation of clock genes.
2004,
Pubmed
He,
CKI and CKII mediate the FREQUENCY-dependent phosphorylation of the WHITE COLLAR complex to close the Neurospora circadian negative feedback loop.
2006,
Pubmed
Huang,
Protein kinase A and casein kinases mediate sequential phosphorylation events in the circadian negative feedback loop.
2007,
Pubmed
Kaneko,
Neuroanatomy of cells expressing clock genes in Drosophila: transgenic manipulation of the period and timeless genes to mark the perikarya of circadian pacemaker neurons and their projections.
2000,
Pubmed
Kim,
Balance between DBT/CKIepsilon kinase and protein phosphatase activities regulate phosphorylation and stability of Drosophila CLOCK protein.
2006,
Pubmed
Kim,
A DOUBLETIME kinase binding domain on the Drosophila PERIOD protein is essential for its hyperphosphorylation, transcriptional repression, and circadian clock function.
2007,
Pubmed
Kivimäe,
Activating PER repressor through a DBT-directed phosphorylation switch.
2008,
Pubmed
Kloss,
Phosphorylation of period is influenced by cycling physical associations of double-time, period, and timeless in the Drosophila clock.
2001,
Pubmed
Kloss,
The Drosophila clock gene double-time encodes a protein closely related to human casein kinase Iepsilon.
1998,
Pubmed
Ko,
Role for Slimb in the degradation of Drosophila Period protein phosphorylated by Doubletime.
2002,
Pubmed
Lee,
Posttranslational mechanisms regulate the mammalian circadian clock.
2001,
Pubmed
Lin,
A role for casein kinase 2alpha in the Drosophila circadian clock.
,
Pubmed
Lowrey,
Positional syntenic cloning and functional characterization of the mammalian circadian mutation tau.
2000,
Pubmed
Martinek,
A role for the segment polarity gene shaggy/GSK-3 in the Drosophila circadian clock.
2001,
Pubmed
Meng,
Setting clock speed in mammals: the CK1 epsilon tau mutation in mice accelerates circadian pacemakers by selectively destabilizing PERIOD proteins.
2008,
Pubmed
Meyer,
PER-TIM interactions in living Drosophila cells: an interval timer for the circadian clock.
2006,
Pubmed
Muskus,
Drosophila DBT lacking protein kinase activity produces long-period and arrhythmic circadian behavioral and molecular rhythms.
2007,
Pubmed
Nakajima,
Reconstitution of circadian oscillation of cyanobacterial KaiC phosphorylation in vitro.
2005,
Pubmed
Nawathean,
The doubletime and CKII kinases collaborate to potentiate Drosophila PER transcriptional repressor activity.
2004,
Pubmed
Nawathean,
A small conserved domain of Drosophila PERIOD is important for circadian phosphorylation, nuclear localization, and transcriptional repressor activity.
2007,
Pubmed
Pregueiro,
The Neurospora checkpoint kinase 2: a regulatory link between the circadian and cell cycles.
2006,
Pubmed
Preuss,
Drosophila doubletime mutations which either shorten or lengthen the period of circadian rhythms decrease the protein kinase activity of casein kinase I.
2004,
Pubmed
,
Xenbase
Price,
Suppression of PERIOD protein abundance and circadian cycling by the Drosophila clock mutation timeless.
1995,
Pubmed
Price,
double-time is a novel Drosophila clock gene that regulates PERIOD protein accumulation.
1998,
Pubmed
Rivers,
Regulation of casein kinase I epsilon and casein kinase I delta by an in vivo futile phosphorylation cycle.
1998,
Pubmed
Rothenfluh,
Short-period mutations of per affect a double-time-dependent step in the Drosophila circadian clock.
2000,
Pubmed
Rothenfluh,
A TIMELESS-independent function for PERIOD proteins in the Drosophila clock.
2000,
Pubmed
Sathyanarayanan,
Posttranslational regulation of Drosophila PERIOD protein by protein phosphatase 2A.
2004,
Pubmed
Schafmeier,
Transcriptional feedback of Neurospora circadian clock gene by phosphorylation-dependent inactivation of its transcription factor.
2005,
Pubmed
Sekine,
Casein kinase I epsilon does not rescue double-time function in Drosophila despite evolutionarily conserved roles in the circadian clock.
2008,
Pubmed
Shafer,
Sequential nuclear accumulation of the clock proteins period and timeless in the pacemaker neurons of Drosophila melanogaster.
2002,
Pubmed
Suri,
Two novel doubletime mutants alter circadian properties and eliminate the delay between RNA and protein in Drosophila.
2000,
Pubmed
Vanselow,
Differential effects of PER2 phosphorylation: molecular basis for the human familial advanced sleep phase syndrome (FASPS).
2006,
Pubmed
Vielhaber,
Nuclear entry of the circadian regulator mPER1 is controlled by mammalian casein kinase I epsilon.
2000,
Pubmed
Vosshall,
Block in nuclear localization of period protein by a second clock mutation, timeless.
1994,
Pubmed
Xu,
Functional consequences of a CKIdelta mutation causing familial advanced sleep phase syndrome.
2005,
Pubmed
Yu,
PER-dependent rhythms in CLK phosphorylation and E-box binding regulate circadian transcription.
2006,
Pubmed
