The mouse Clock mutation behaves as an antimorph and maps within the W19H deletion, distal of Kit.
Clock is a semidominant mutation identified from an N-ethyl-N-nitrosourea mutagenesis screen in mice. Mice carrying the Clock mutation exhibit abnormalities of circadian behavior, including lengthening of endogenous period and loss of rhythmicity. To identify the gene affected by this mutation, we have generated a high-resolution genetic map (> 1800 meioses) of the Clock locus. We report that Clock is 0.7 cM distal of Kit on mouse chromosome 5. Mapping shows that Clock lies within the W19H deletion. Complementation analysis of different Clock and W19H compound genotypes indicates that the Clock mutation behaves as an antimorph. This antimorphic behavior of Clock strongly argues that Clock defines a gene centrally involved in the mammalian circadian system.
King
D P
DP
National Science Foundation Center for Biological Timing, Northwestern University, Evanston, Illinois 60208-3520, USA.
Vitaterna
M H
MH
Chang
A M
AM
Dove
W F
WF
Pinto
L H
LH
Turek
F W
FW
Takahashi
J S
JS
D000818:Animals; D056926:CLOCK Proteins; D002874:Chromosome Mapping; D002940:Circadian Rhythm; D005260:Female; D017353:Gene Deletion; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008809:Mice, Inbred C3H; D008810:Mice, Inbred C57BL; D009154:Mutation; D010641:Phenotype; D019009:Proto-Oncogene Proteins c-kit / Q000235:genetics; D015534:Trans-Activators / Q000235:genetics*
D015534:Trans-Activators; D056926:CLOCK Proteins; C538944:Clock protein, mouse; D019009:Proto-Oncogene Proteins c-kit