in mammals, mper2 forms a heterodimer with mper1, mcry1, and mcry2 by binding to pas domains. the heterodimer acts to inhibit their own transcription by suppressing the clock/bmal1 complex resulting in a negative feedback loop. this negative feedback loop is essential for maintaining a functioning circadian clock. a disruption of either both mper1 and mper2 genes together or both mcry genes causes behavioural arrhythmicity when the double-knockout animals are placed in constant conditions. a third per gene, "mper3", does not have a critical role in the maintenance of the core clock feedback loops. molecular and behavioural rhythms are preserved in mice lacking m"per3".