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Molecular and Cellular Biology, December 2001, p. 8329-8335, Vol. 21, No. 24
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.24.8329-8335.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Loss of mRor1 Enhances the Heart and Skeletal Abnormalities in mRor2-Deficient Mice: Redundant and Pleiotropic Functions of mRor1 and mRor2 Receptor Tyrosine Kinases

Masashi Nomi,1 Isao Oishi,1 Shuichi Kani,1 Hiroaki Suzuki,1 Takeru Matsuda,1 Akinori Yoda,1 Makiko Kitamura,2 Kyoko Itoh,2 Shigeto Takeuchi,1 Kiyoshi Takeda,3 Shizuo Akira,3 Makoto Ikeya,4,dagger Shinji Takada,4,5 and Yasuhiro Minami1,*

Department of Genome Sciences1 and Department of Biomedical Informatics,2 Kobe University, Graduate School of Medicine, Kobe 650-0017, Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka 565-0871,3 Center for Molecular and Developmental Biology, Graduate School of Science, Kyoto University, Sakyo-ku, Kyoto 606-8502,4 and Kondoh Differentiation Signalling Project, ERATO (Exploratory Research for Advanced Technology) of Japan Science and Technology Corporation (JST), Sakyo-ku, Kyoto 606-8305,5 Japan

Received 25 June 2001/Accepted 10 September 2001

The mammalian Ror family of receptor tyrosine kinases consists of two structurally related proteins, Ror1 and Ror2. We have shown that mRor2-deficient mice exhibit widespread skeletal abnormalities, ventricular septal defects in the heart, and respiratory dysfunction, leading to neonatal lethality (S. Takeuchi, K. Takeda, I. Oishi, M. Nomi, M. Ikeya, K. Itoh, S. Tamura, T. Ueda, T. Hatta, H. Otani, T. Terashima, S. Takada, H. Yamamura, S. Akira, and Y. Minami, Genes Cells 5:71-78, 2000). Here we show that mRor1-deficient mice have no apparent skeletal or cardiac abnormalities, yet they also die soon after birth due to respiratory dysfunction. Interestingly, mRor1/mRor2 double mutant mice show markedly enhanced skeletal abnormalities compared with mRor2 mutant mice. Furthermore, double mutant mice also exhibit defects not observed in mRor2 mutant mice, including a sternal defect, dysplasia of the symphysis of the pubic bone, and complete transposition of the great arteries. These results indicate that mRor1 and mRor2 interact genetically in skeletal and cardiac development.

* Corresponding author. Mailing address: Department of Genome Sciences (Division of Biomedical Regulation), Kobe University, Graduate School of Medicine, 7-5-1, Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan. Phone: 81-78-382-5560. Fax: 81-78-382-5579. E-mail: minami{at}kobe-u.ac.jp.

dagger Present address: Department of Medical Embryology and Neurobiology, Institute for Frontier Medical Science, Kyoto University, Sakyo-ku, Kyoto 606-8507, Japan.

Molecular and Cellular Biology, December 2001, p. 8329-8335, Vol. 21, No. 24
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.24.8329-8335.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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