Melatonin and wheel running rhythmicity and the effects of acute and chronic light pulses on these rhythms were studied in Clock ¹⁹ mutant mice selectively bred to synthesise melatonin. Homozygous melatonin proficient Clock ¹⁹ mutant mice (Clock ^19/19-MEL) produced melatonin rhythmically with peak production 2 hours later than the wild type controls (ie just prior to the time of lights on). By contrast the time of onset of wheel running activity occurred within a 20 minute period around lights off irrespective of the genotype. The melatonin production in the mutants spontaneously decreased within 1 hour of the expected time of lights on. Upon placing the mice in continuous darkness, the melatonin rhythm persisted and the peak occurred 2 hours later each cycle over the first 2 cycles, consistent with the endogenous period of the mutant. This contrasted with the onset of wheel running activity, which did not shift for several days in constant darkness. A light pulse around the time of expected lights on, followed by constant darkness reduced the expected 2 hour delay of the melatonin peak of the mutants to about 1 hour while causing an advance in the time of the melatonin peak in the wild type mice. When the Clock ^19/19-MEL mice were maintained in a skeleton photoperiod of daily 15 minute light pulses, a higher proportion entrained to the schedule (57%) than melatonin deficient mutants (9%). These results provide compelling evidence that mice with the Clock ¹⁹ mutation express essentially normal rhythmicity albeit with an underlying endogenous period of 26 - 27 hours and they can be entrained by brief exposure to light. They also raise important questions about the role of Clock in rhythmicity and the usefulness of behavioural rhythm monitoring compared to hormonal rhythms.