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Abstract
Mice carrying a null mutation in the Period 1 (mPer1) gene were generated using embryonic
stem cell technology. Homozygous mPer1 mutants display a shorter circadian period
with reduced precision and stability. Mice deficient in both mPer1 and mPer2 do not
express circadian rhythms. While mPER2 regulates clock gene expression at the transcriptional
level, mPER1 is dispensable for the rhythmic RNA expression of mPer1 and mPer2 and
may instead regulate mPER2 at a posttranscriptional level. Studies of clock-controlled
genes (CCGs) reveal a complex pattern of regulation by mPER1 and mPER2, suggesting
independent controls by the two proteins over some output pathways. Genes encoding
key enzymes in heme biosynthesis are under circadian control and are regulated by
mPER1 and mPER2. Together, our studies show that mPER1 and mPER2 have distinct and
complementary roles in the mouse clock mechanism.