Abstract
Several non-clock functions of clock genes have been discovered. In mammals, the circadian system and stress systems, both centers of which are located in the hypothalamus, are involved in an adaptation to predictable and unpredictable environmental stimuli, respectively. Although the interaction and relationship between these 2 systems are intriguing and have been studied in different ways since the "pre-clock-gene" era, the molecular interaction between them largely remains unknown. I show by systematic molecular biological analysis that acute physical stress elevated only Period1 (Per1) mRNA expression in mouse peripheral organs. Although behavioral rhythms in vivo and peripheral molecular clocks are rather stable against acute restraint stress, the results of a series of promoter analyses, including chromatin immunoprecipitation (ChIP) assays, indicate that a glucocorticoid responsive element (GRE) in the Per1 promoter is indispensable for induction of this mRNA both in vitro and in vivo. These results suggest that Per1 can be a potential stress marker and that there may exist a third pathway of Per1 transcriptional control in addition to the clock-regulated BMAL1/CLOCK-E-box and light-responsive CREB-CRE pathways. [J Physiol Sci. 2006;56 Suppl:S15]
