Mouse period1(mPer1) andmPer2are mammalian homologs of theDrosophilaclock geneperiodthat show robust oscillation in the suprachiasmatic nucleus, the mammalian master clock, and have been implicated as essential components of the core clock mechanism. Gene-targeting studies have demonstrated thatmPer2plays a dominant function in behavioral rhythm generation, although the role ofmPer1has not been fully clarified. Here, we report that prolongation of the lighting period (4-16 h) induces a larger-delay phase shift of the behavioral rhythm inmPer1-deficient (mPer1-/-) mice. During the light-elongation task, mPER2 protein decay inmPer1-/-mice is slower (∼4 h) than in wild-type mice, which thereby causes larger behavioral phase delay.mPer1-/-mice could not adapt to environmental light/dark cycles in long complete photoperiods with dim light or in long skeleton photoperiods. These photoperiodic conditions mimic natural environmental changes present at high latitudes, indicating thatmPer1could operate in the adaptation of the circadian clock of nocturnal mice to large seasonal changes of environmental light/dark cycles.