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J. Biol. Chem., Vol. 282, Issue 51, 37285-37292, December 21, 2007

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Heat Shock Transcription Factor 1 Is Required for Maintenance of Ciliary Beating in Mice^*

Eiichi Takaki, Mitsuaki Fujimoto, Takashi Nakahari, Shigenobu Yonemura^¶, Yoshihiko Miyata^||, Naoki Hayashida, Kaoru Yamamoto, Richard B. Vallee^**, Tsuyoshi Mikuriya, Kazuma Sugahara, Hiroshi Yamashita, Sachiye Inouye, and Akira Nakai¹

From the Biochemistry and Molecular Biology and Otolaryngology, Yamaguchi University School of Medicine, Ube 755-8505, Japan, the Department of Physiology, Osaka Medical College, Takatsuki, Osaka 569-8686, Japan, the ^¶Laboratory for Cellular Morphogenesis, RIKEN Center for Developmental Biology, Kobe 650-0047, Japan, the ^||Department of Cell and Developmental Biology, Graduate School of Biostudies, Kyoto University, Kyoto 606-8502, Japan, and the ^**Department of Pathology, College of Physicians and Surgeons, Columbia University, New York, New York 10032

Heat shock transcription factors (HSFs) maintain protein homeostasis through regulating expression of heat shock proteins, especially in stressed conditions. In addition, HSFs are involved in cellular differentiation and development by regulating development-related genes, as well as heat shock genes. Here, we showed chronic sinusitis and mild hydrocephalus in postnatal HSF1-null mice, which are associated with impaired mucociliary clearance and cerebrospinal flow, respectively. Analysis of ciliary beating revealed that the amplitude of the beating was significantly reduced, and ciliary beat frequencies were lower in the respiratory epithelium, ependymal cells, oviduct, and trachea of HSF1-null mice than those of wild-type mice. Cilia possess a common axonema structure composed of microtubules of - and β-tubulin. We found a marked reduction in - and ciliary β_iv-tubulin in the HSF1-null cilia, which is developmentally associated with reduced Hsp90 expression in HSF1-null mice. Treatment of the respiratory epithelium with geldanamycin resulted in rapid reduction of ciliary beating in a dose-dependent manner. Furthermore, Hsp90 was physically associated with ciliary β_iv-tubulin, and Hsp90 stabilizes tubulin polymerization in vitro. These results indicate that HSF1 is required to maintain ciliary beating in postnatal mice, probably by regulating constitutive expression of Hsp90 that is important for tubulin polymerization.

Received for publication, June 4, 2007 , and in revised form, October 23, 2007.

^* This work was supported in part by Grants-in-aid for Scientific Research and on Priority Areas-a Nuclear System of DECODE and Life of Proteins, from the Ministry of Education, Culture, Sports, Science and Technology, Japan, the Uehara Foundation, NOVARTIS Foundation, Nakatomi Foundation, 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.

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

¹ To whom correspondence should be addressed. Tel.: 81-836-22-2214; Fax: 81-836-22-2315; E-mail: anakai{at}yamaguchi-u.ac.jp.

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