International Mammalian Genome Society

The 14th International Mouse Genome Conference (2000)

H18. Mutant Mice Lacking Crk-II Caused by Gene Trap Insertional Mutagenesis: Crk-II Is Not Essential for Embryonic Development

Tomohisa Sekimoto1,4, Takashi Imaizumi1, Katsutaka Miura1, Masatake Araki2, Misao Suzuki3, Naoya Tajima4, Kimi Araki1, Ken-ichi Yamamura1,3
1 Dept. of Developmental Genetics, Institute of Molecular Embryology and Genetics, Kumamoto University School of Medicine, 2Gene Technology Center, 3Center for Animal Resources and Development, Kumamoto University, Kumamoto, Japan. 4Dept. of Orthopaedics Surgery, Miyazaki Medical College, Miyazaki, Japan.

Crk family adapter proteins including Crk-II, Crk-I and Crk-L consist mostly of SH2 and SH3 domains. Through the interactions between the SH2 domain and phosphotyrosine residues and/or between the SH3 domain and proline-rich motifs, they are involved in a variety of signaling cascades. Despite their essential roles in signal transduction, knock-out mice as to these molecules have not been reported yet. We performed gene trap insertional mutagenesis with a trap vector, pU-Hachi, and generated a mutant mice line, Ayu 8104, in which the trap vector is inserted into the c-crk gene. Homozygous Ayu 8104 mice lacked Crk-II and Crk-I transcripts but expressed truncated Crk proteins retaining one SH2 and one SH3 domain. Since the structures of the truncated proteins were similar to that of Crk-I, the insertion was considered to cause Crk-II specific disruption. Homozygous mutant mice, however, did not exhibit any obvious abnormalities, suggesting that Crk-family adapters, Crk-II, Crk-I and Crk-L would redundantly function in the signaling cascades and that Crk-II is not apparently essential for embryonic development.

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