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Molecular and Cellular Biology, May 2001, p. 3343-3350, Vol. 21, No. 10
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.10.3343-3350.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Six4, a Putative myogenin Gene Regulator, Is Not Essential for Mouse Embryonal Development

Hidenori Ozaki,1 Yoko Watanabe,1 Katsumasa Takahashi,2 Ken Kitamura,2,dagger Akira Tanaka,3 Koko Urase,4 Takashi Momoi,4 Katsuko Sudo,5 Junko Sakagami,5 Masahide Asano,5,Dagger Yoichiro Iwakura,5 and Kiyoshi Kawakami1,*

Departments of Biology,1 Otolaryngology,2 and Pathology,3 Jichi Medical School, Tochigi 329-0498, Division of Development and Differentiation, National Institute of Neuroscience, NCNP, Kodaira, Tokyo 187-8502,4 and Division of Cell Biology, Center for Experimental Medicine, Institute of Medical Science, University of Tokyo, Tokyo 108-8639,5 Japan

Received 27 November 2000/Returned for modification 9 January 2001/Accepted 21 February 2001

Six4 is a member of the Six family genes, homologues of Drosophila melanogaster sine oculis. The gene is thought to be involved in neurogenesis, myogenesis, and development of other organs, based on its specific expression in certain neuronal cells of the developing embryo and in adult skeletal muscles. To elucidate the biological roles of Six4, we generated Six4-deficient mice by replacing the Six homologous region and homeobox by the beta -galactosidase gene. 5-Bromo-4-chloro-3-indolyl-beta -D-galactopyranoside staining of the heterozygous mutant embryos revealed expression of Six4 in cranial and dorsal root ganglia, somites, otic and nasal placodes, branchial arches, Rathke's pouch, apical ectodermal ridges of limb buds, and mesonephros. The expression pattern was similar to that of Six1 except at the early stage of embryonic day 8.5. Six4-deficient mice were born according to the Mendelian rule with normal gross appearance and were fertile. No hearing defects were detected. Six4-deficient embryos showed no morphological abnormalities, and the expression patterns of several molecular markers, e.g., myogenin and NeuroD3 (neurogenin1), were normal. Our results indicate that Six4 is not essential for mouse embryogenesis and suggest that other members of the Six family seem to compensate for the loss of Six4.

* Corresponding author. Mailing address: Department of Biology, Jichi Medical School, 3311-1 Yakushiji, Minamikawachi, Kawachi, Tochigi 329-0498, Japan. Phone: 81 (285) 58-7311. Fax: 81 (285) 44-5476. E-mail: kkawakam{at}jichi.ac.jp.

dagger Present address: Department of Otolaryngology, Tokyo Medical and Dental University, Tokyo 113-8519, Japan.

Dagger Present address: Institute for Experimental Animals, Faculty of Medicine, Kanazawa University, Kanazawa 920-8640, Japan.

Molecular and Cellular Biology, May 2001, p. 3343-3350, Vol. 21, No. 10
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.10.3343-3350.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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