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J. Biol. Chem., Vol. 281, Issue 8, 4931-4937, February 24, 2006

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Maintenance of Olfactory Neurogenesis Requires HSF1, a Major Heat Shock Transcription Factor in Mice^*

Eiichi Takaki, Mitsuaki Fujimoto, Kazuma Sugahara, Takashi Nakahari^¶, Shigenobu Yonemura^||, Yasunori Tanaka, Naoki Hayashida, Sachiye Inouye, Tsuyoshi Takemoto, Hiroshi Yamashita, and Akira Nakai¹

From the Departments of Biochemistry and Molecular Biology and Otolaryngology, Yamaguchi University School of Medicine, Ube 755-8505, Japan, ^¶Department of Physiology, Osaka Medical College, Takatsuki, Osaka 569-8686, Japan, and ^||Laboratory for Cellular Morphogenesis, RIKEN Center for Developmental Biology, Kobe 650-0047, Japan

Heat shock transcription factors (HSFs) play roles not only in heat shock response but also in development of the reproductive organs, brain, and lens. Here, we analyzed sensory organs and found abnormalities of the olfactory epithelium in adult HSF1-null mice, which is developmentally related to the lens. The olfactory epithelium was normal until postnatal 3 weeks but was not maintained later than 4 weeks in HSF1-null mice. The olfactory epithelium was atrophied with increased cell death of olfactory sensory neurons. Analysis of the epithelium revealed that induction of HSP expression and reduction of LIF expression are lacking in adult HSF1-null mice. We found that DNA binding activity of HSF1 is induced in the olfactory epithelium later than 4 weeks and that HSF1 binds directly to Lif gene and inhibits its expression. HSF4 has opposing effects on LIF expression and olfactory neurogenesis. These data indicate that HSF1 is required for the precise expression of Hsp and cytokine genes that is obligatory for maintenance of olfactory neurogenesis in adult mice and suggest that stress-related processes are involved in its maintenance.

Received for publication, June 14, 2005 , and in revised form, October 31, 2005.

^* This work was supported in part by grants-in-aid for scientific research and on priority areas from the Ministry of Education, Culture, Sports, Science, and Technology, Japan, the Uehara Foundation, the NOVARTIS Foundation, the Nakatomi Foundation, the Kao Foundation for Arts and Sciences, and the Yamaguchi University 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.

¹ To whom correspondence should be addressed: Dept. of Biochemistry and Molecular Biology, Yamaguchi University School of Medicine, Minami-Kogushi 1-1-1, Ube 755-8505, Japan. Tel.: 81-836-22-2214; Fax: 81-836-22-2315; E-mail: anakai{at}yamaguchi-u.ac.jp.

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