<i>Six1</i>controls patterning of the mouse otic vesicle

• Hidenori Ozaki

  Division of Biology, Center for Molecular Medicine, Jichi Medical School,Tochigi 329-0498, Japan

• Kazuaki Nakamura

  Division of Biology, Center for Molecular Medicine, Jichi Medical School,Tochigi 329-0498, Japan

• Jun-ichi Funahashi

  Department of Molecular Neurobiology, Institute of Development, Aging and Cancer, Tohoku University, Sendai 980-8575, Japan

• Keiko Ikeda

  Division of Biology, Center for Molecular Medicine, Jichi Medical School,Tochigi 329-0498, Japan

• Gen Yamada

  Division of Transgenic Technology, Center for Animal Resources and Development, Kumamoto University, Kumamoto 860-0811, Japan

• Hisashi Tokano

  Department of Otolaryngology, Tokyo Medical and Dental University, Tokyo 113-8519, Japan

• Hiro-oki Okamura

  Department of Otolaryngology, Tokyo Medical and Dental University, Tokyo 113-8519, Japan

• Ken Kitamura

  Department of Otolaryngology, Tokyo Medical and Dental University, Tokyo 113-8519, Japan

• Shigeaki Muto

  Division of Nephrology, Department of Internal Medicine, Jichi Medical School,Tochigi 329-0498, Japan

• Hayato Kotaki

  Division of Cell Biology, Center for Experimental Medicine, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan

• Katsuko Sudo

  Division of Cell Biology, Center for Experimental Medicine, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan

• Reiko Horai

  Division of Cell Biology, Center for Experimental Medicine, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan

• Yoichiro Iwakura

  Division of Cell Biology, Center for Experimental Medicine, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan

• Kiyoshi Kawakami

  Division of Biology, Center for Molecular Medicine, Jichi Medical School,Tochigi 329-0498, Japan

抄録

Six1 is a member of the Six family homeobox genes, which function as components of the Pax-Six-Eya-Dach gene network to control organ development. Six1 is expressed in otic vesicles, nasal epithelia,branchial arches/pouches, nephrogenic cords, somites and a limited set of ganglia. In this study, we established Six1-deficient mice and found that development of the inner ear, nose, thymus, kidney and skeletal muscle was severely affected. Six1-deficient embryos were devoid of inner ear structures, including cochlea and vestibule, while their endolymphatic sac was enlarged. The inner ear anomaly began at around E10.5 and Six1was expressed in the ventral region of the otic vesicle in the wild-type embryos at this stage. In the otic vesicle of Six1-deficient embryos,expressions of Otx1, Otx2, Lfng and Fgf3,which were expressed ventrally in the wild-type otic vesicles, were abolished,while the expression domains of Dlx5, Hmx3, Dach1and Dach2, which were expressed dorsally in the wild-type otic vesicles, expanded ventrally. Our results indicate that Six1functions as a key regulator of otic vesicle patterning at early embryogenesis and controls the expression domains of downstream otic genes responsible for respective inner ear structures. In addition, cell proliferation was reduced and apoptotic cell death was enhanced in the ventral region of the otic vesicle, suggesting the involvement of Six1 in cell proliferation and survival. In spite of the similarity of otic phenotypes of Six1- and Shh-deficient mice, expressions of Six1 and Shhwere mutually independent.

収録刊行物

• Development

  Development 131 (3), 551-562, 2004-02-01

  The Company of Biologists

キーワード

• Developmental Biology
• Molecular Biology

詳細情報

• CRID: 1363951793764761728
• NII論文ID: 30002332671
• DOI: 10.1242/dev.00943
• ISSN: 14779129
• ISSN: 09501991
• Web Site: http://journals.biologists.com/dev/article-pdf/131/3/551/1147990/551.pdf
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