TY - JOUR
T1 - A mutant Drosophila homolog of mammalian clock disrupts circadian rhythms and transcription of period and timeless
AU - Allada, Ravi
AU - White, Neal E.
AU - So, W. Venus
AU - Hall, Jeffrey C.
AU - Rosbash, Michael
N1 - Funding Information:
We thank G. Fasciani for performing the optomotor tests; C. Kotarski for assistance with sequencing, oligonucleotide synthesis and Northern blot preparation; L. Sarov-Blat for Northern analysis; the Brandeis/HHMI Sequencing Facility, Harvard Biopolymer Facility for assistance with sequencing; V. Suri for identification of the EST and sequence analysis; J. Rutila, M. Le, and S. Goodwin for helpful discussions; A. Rourke for fly crosses and maintenance; L.-A. Monaghan for assistance with manuscript preparation; T. Schwarz, B. Hamilton, and J. Huang for cDNA libraries; Berkeley Drosophila Genome Project and S. Artavonas-Tsakonas for P1 clones; K. Wager-Smith and S. Kay for sharing results prior to publication; and Bloomington (IN) Stock Center for fly strains. This work was supported by grants from NSF, Center for Biological Timing, NIH to M. Rosbash and J. C. Hall and an HHMI Postdoctoral Research Fellowship for Physicians (R. A.).
PY - 1998/5/29
Y1 - 1998/5/29
N2 - We report the identification, characterization, and cloning of a novel Drosophila circadian rhythm gene, dClock. The mutant, initially called Jrk, manifests dominant effects: heterozygous flies have a period alteration and half are arrhythmic, while homozygous flies are uniformly arrhythmic. Furthermore, these flies express low levels of the two clock proteins, PERIOD (PER) and TIMELESS (TIM), due to low per and tim transcription. Mapping and cloning of the Jrk gene indicates that it encodes the Drosophila homolog of mouse Clock. The mutant phenotype results from a premature stop codon that eliminates much of the putative activation domain of this bHLH-PAS transcription factor, thus explaining the dominant features of Jrk. The remarkable sequence conservation strongly supports common clock components present in the common ancestor of Drosophila and mammals.
AB - We report the identification, characterization, and cloning of a novel Drosophila circadian rhythm gene, dClock. The mutant, initially called Jrk, manifests dominant effects: heterozygous flies have a period alteration and half are arrhythmic, while homozygous flies are uniformly arrhythmic. Furthermore, these flies express low levels of the two clock proteins, PERIOD (PER) and TIMELESS (TIM), due to low per and tim transcription. Mapping and cloning of the Jrk gene indicates that it encodes the Drosophila homolog of mouse Clock. The mutant phenotype results from a premature stop codon that eliminates much of the putative activation domain of this bHLH-PAS transcription factor, thus explaining the dominant features of Jrk. The remarkable sequence conservation strongly supports common clock components present in the common ancestor of Drosophila and mammals.
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U2 - 10.1016/S0092-8674(00)81440-3
DO - 10.1016/S0092-8674(00)81440-3
M3 - Article
C2 - 9630223
AN - SCOPUS:17044451254
VL - 93
SP - 791
EP - 804
JO - Cell
JF - Cell
SN - 0092-8674
IS - 5
ER -