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Molecular and Cellular Biology, April 2003, p. 2489-2500, Vol. 23, No. 7
0270-7306/03/$08.00+0     DOI: 10.1128/MCB.23.7.2489-2500.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Functional Analysis of Basic Transcription Element Binding Protein by Gene Targeting Technology

Masanobu Morita,1,{dagger} Akira Kobayashi,1,{ddagger} Toshiharu Yamashita,1,{ddagger} Tomomasa Shimanuki,1 Osamu Nakajima,2 Satoru Takahashi,2 Shiro Ikegami,3 Kaoru Inokuchi,3 Keisuke Yamashita,4 Masayuki Yamamoto,2 and Yoshiaki Fujii-Kuriyama1,5*

Department of Biomolecular Science, Graduate School of Life Science, Tohoku University, Sendai 980-8578,1 Center for Tsukuba Advanced Research Alliance and Institute for Basic Medical Sciences, University of Tsukuba, Tsukuba 305-8577,2 Mitsubishi Kagaku Institute of Life Sciences, Machida, Tokyo 194-8511,3 Department of Anatomy and Developmental Biology, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima 734-8551,4 Core Research for Evolutionary Science and Technology, Japan Science and Technology, Tokyo, Japan5

Received 14 June 2002/ Returned for modification 7 October 2002/ Accepted 19 December 2002

Basic transcription element binding protein (BTEB) is a transcription factor with a characteristic zinc finger motif and is most remarkably enhanced by thyroid hormone T3 treatment (R. J. Denver et al., J. Biol. Chem. 272:8179-8188, 1997). To investigate the function of BTEB per se and to touch on the effects of T3 (3,5,3'-triiodothyronine) on mouse development, we generated BTEB-deficient mice by gene knockout technology. Homologous BTEB-/- mutant mice were bred according to apparently normal Mendelian genetics, matured normally, and were fertile. Mutant mice could survive for at least 2 years without evident pathological defects. From the expression of lacZ, which was inserted into the reading frame of the BTEB gene, BTEB showed a characteristic tissue-specific expression profile during the developmental process of brain and bone. Dramatically increased expression of BTEB was observed in Purkinje cells of the cerebellum and pyramidal cell layers of the hippocampus at P7 when synapses start to form in the brain. Although general behavioral activities such as locomotion, rearing, and speed of movement were not so much affected in the BTEB-/- mutant mice, they showed clearly reduced activity levels in rotorod and contextual fear-conditioning tests; this finding was probably due to defective functions of the cerebellum, hippocampus, and amygdala.

* Corresponding author. Mailing address: TARA Center, University of Tsukuba, Tennoudai 1-1-1, Tsukuba, Ibaraki 305-8577, Japan. Phone: 81-298-53-7323. Fax: 81-298-53-7318. E-mail: ykfujii{at}tara.tskuba.ac.jp.

{dagger} Present address: The Salk Institute for Biological Studies, La Jolla, CA 92037-1099.

{ddagger} Present address: Center for Tsukuba Advanced Research Alliance and Institute for Basic Medical Sciences, University of Tsukuba, Tsukuba, Ibaraki 305-8577, Japan.

Molecular and Cellular Biology, April 2003, p. 2489-2500, Vol. 23, No. 7
0022-538X/03/$08.00+0     DOI: 10.1128/MCB.23.7.2489-2500.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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