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Abstract
The role of mPer1 and mPer2 in regulating circadian rhythms was assessed by disrupting
these genes. Mice homozygous for the targeted allele of either mPer1 or mPer2 had
severely disrupted locomotor activity rhythms during extended exposure to constant
darkness. Clock gene RNA rhythms were blunted in the suprachiasmatic nucleus of mPer2
mutant mice, but not of mPER1-deficient mice. Peak mPER and mCRY1 protein levels were
reduced in both lines. Behavioral rhythms of mPer1/mPer3 and mPer2/mPer3 double-mutant
mice resembled rhythms of mice with disruption of mPer1 or mPer2 alone, respectively,
confirming the placement of mPer3 outside the core circadian clockwork. In contrast,
mPer1/mPer2 double-mutant mice were immediately arrhythmic. Thus, mPER1 influences
rhythmicity primarily through interaction with other clock proteins, while mPER2 positively
regulates rhythmic gene expression, and there is partial compensation between products
of these two genes.