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Genetic and molecular approaches have been critical for elucidating the mechanism of the mammalian circadian clock. Here, we demonstrate that the  ClockΔ19  mutant behavioral phenotype is significantly modified by mouse strain genetic background. We map a suppressor of the  ClockΔ19  mutation to a ∼900 kb interval on mouse chromosome 1 and identify the transcription factor,  Usf1 , as the responsible gene. A SNP in the promoter of  Usf1  causes elevation of its transcript and protein in strains that suppress the  Clock  mutant phenotype. USF1 competes with the CLOCK:BMAL1 complex for binding to E-box sites in target genes. Saturation binding experiments demonstrate reduced affinity of the CLOCKΔ19:BMAL1 complex for E-box sites, thereby permitting increased USF1 occupancy on a genome-wide basis. We propose that USF1 is an important modulator of molecular and behavioral circadian rhythms in mammals.

Usf1 , a suppressor of the circadian Clock mutant, reveals the nature of the DNA-binding of the CLOCK:BMAL1 complex in mice