Casein kinases (CK) are central regulators of the circadian clock. Mutations in CK1 and its target hPer2 cause sleep disorders in patients whilst the tau mutation of CK1e in hamsters accelerates circadian rest/activity cycles and amplifies resetting responses to light. We re-created this mutation in mice and also generated whole-animal knock-outs by using the Cre-loxP system. Tau mutant mice express robust, short period circadian rest/activity rhythms comparable to mutant hamsters and patients, although re-setting responses to light are normal. In contrast, circadian period is lengthened in knock-out animals. Multi- and single-unit recording of SCN firing rates revealed periods comparable to genotype-specific behaviour. Clock gene mRNA and protein rhythms were also accelerated in both SCN and peripheral tissues, revealing for the first time the global impact of the mutation on the molecular pacemaker, and supporting a model of CK1e^tau as a gain of function accelerating clock protein turnover during circadian night. Studies of PER2 protein turnover using luciferase imaging of SCN slices and single cells reveal that circadian phase is accelerated in the early night, compressing this phase by 4 hours, but of normal phase and duration in the subjective day time. These real-time imaging data now reveal for the first time how a circadian mutation accelerates a target protein at a specific phase of the cycle, and support a model for accelerated PERIOD protein turnover in the early nocturnal phase. We extend these data to peripheral tissue in a predictive model which describes the impact of the tau mutation on re-setting responses to external stimuli.