Circadian rhythms are endogenous oscillations of physiological and behavioral phenomena with period length of -24 hr. A mutation in human Period 2 (hPER2), a gene crucial for resetting the central clock in response to light, is associated with familial advanced sleep phase syndrome (FASPS), an autosomal dominant condition with early morning awakening and early sleep times. The FASPS hPER2 S662G mutation resulted in PER2 being hypophosphorylated by casein kinase I (CKI) in vitro. We generated transgenic mice carrying the FASPS hPER2 S662G mutation and faithfully recapitulate the human phenotype. We show that phosphorylation at S662 leads to increased PER2 transcription and suggest that phosphorylation at another site leads to PER2 degradation. Altering CK1 delta dosage modulates the S662 phenotype demonstrating that CK1 delta can regulate period through PER2 in vivo. Modeling a naturally occurring human variant in mice has yielded novel insights into PER2 regulation.

Direct CP violation in nonleptonic hyperon decays can be established by comparing the decays of hyperons and anti-hyperons. For Xi decay to Lambda pi followed by Lambda to p pi, the proton distribution in the rest frame of Lambda is governed by the product of the decay parameters alXi alLam. The asymmetry A_Xi Lambda, proportional to the difference of alXi alLam of the hyperon and anti-hyperon decays, vanishes if CP is conserved. We report on an analysis of a fraction of 1997 and 1999 data collected by the Hyper CP (E871) collaboration during the fixed-target runs at Fermilab. The preliminary measurement of the asymmetry is AXiLam = [ -7 pm 12(rm stat) pm 6.2(rm sys) ] times 10-4, an order of magnitude better than the present limit.