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J. Biol. Chem., Vol. 280, Issue 51, 42036-42043, December 23, 2005

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Acute Physical Stress Elevates Mouse Period1 mRNA Expression in Mouse Peripheral Tissues via a Glucocorticoid-responsive Element^*

Takuro Yamamoto¶1, Yasukazu Nakahata1, Masami Tanaka||, Mayumi Yoshida||, Haruhiko Soma, Kazuyuki Shinohara**, Akio Yasuda, Takayoshi Mamine, and Toru Takumi¶2

From the Osaka Bioscience Institute, Suita, Osaka 565-0874, Japan, the Life Science Laboratory, Materials Laboratories, Sony Corporation, Shinagawa, Tokyo 144-0001, Japan, the ^¶Graduate School of Medicine, Osaka City University, Osaka 545-8585, Japan, the Graduate Schools of ^||Biostudies and Medicine, Kyoto University, Sakyo, Kyoto 606-8501, Japan, and the ^**Department of Physiology, Graduate School of Medicine, Nagasaki University, Nagasaki 852-8523, Japan

In mammals, the circadian and stress systems (both centers of which are located in the hypothalamus) are involved in adaptation to predictable and unpredictable environmental stimuli, respectively. Although the interaction and relationship between these two systems are intriguing and have been studied in different ways since the "pre-clock gene" era, the molecular interaction between them remains largely unknown. Here, we 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 assays, indicate that a glucocorticoid-responsive element 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 a third pathway of Per1 transcriptional control may exist in addition to the clock-regulated CLOCK-BMAL1/E-box and light-responsive cAMP-responsive element-binding protein/cAMP-responsive element pathways.

Received for publication, August 31, 2005 , and in revised form, October 19, 2005.

^* This work was supported in part by research grants from the Ministry of Education, Culture, Sports, Science, and Technology and the Takeda Science Foundation. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

The on-line version of this article (available at http://www.jbc.org) contains supplemental Figs. S1 and S2.

¹ Both authors contributed equally to this work.

² To whom correspondence should be addressed: Osaka Bioscience Inst., 6-2-4 Furuedai, Suita, Osaka 565-0874, Japan. Tel.: 81-6-6872-4816; Fax: 81-6-6872-0240; E-mail: takumi{at}obi.or.jp.

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