Assembling a clock for all seasons: Are there M and E oscillators in the genes?

The hypothesis is advanced that the circadian pacemaker in the mammalian su prachiasmatic nucleus (SCN) is composed at the molecular level of a nonredu ndant double complex of circadian genes (per1, cry1, and per2, cry2). Each one of these sets would be sufficient for the maintenance of endogenous rhy thmicity and thus constitute an oscillator. Each would have slightly differ ent temporal dynamics and light responses. The per1/cry1 oscillator is acce lerated by light and decelerated by darkness and thereby tracks dawn when d ay length changes. The per2/cry2 oscillator is decelerated by light and acc elerated by darkness and thereby tracks dusk. These M (morning) and E (even ing) oscillators would give rise to the SCN's neuronal activity in an M and an E component. Suppression of behavioral activity by SCN activity in noct urnal mammals would give rise to adaptive tuning of the endogenous behavior al program to day length. The proposition-which is a specification of Pitte ndrigh and Daan's E-M oscillator model-yields specific nonintuitive predict ions amenable to experimental testing in animals with mutations of circadia n genes.