Mouse period1 (mPer1) and mPer2 are mammalian homologs of the Drosophila clock gene period that 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 that mPer2 plays a dominant function in behavioral rhythm generation, although the role of mPer1 has 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 in mPer1-deficient (mPer1^-/-) mice. During the light-elongation task, mPER2 protein decay in mPer1^-/- 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 that mPer1 could operate in the adaptation of the circadian clock of nocturnal mice to large seasonal changes of environmental light/dark cycles.