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Comparative Genome Mapping of the Ataxia–Telangiectasia Region in Mouse, Rat, and Syrian Hamster
Authors:Yoichi Matsuda    Takashi Imai   Tadahiro Shiomi   Toshiyuki Saito   Masatake Yamauchi   Toshiyuki Fukao   Yukihiro Akao   Naohiko Seki   Hiroko Ito  Tada-aki Hori   
Affiliation:aGenome Research Group, National Institute of Radiological Sciences, 4-9-1 Anagawa, Inage-ku, Chiba, 263, Japan;bDepartment of Pediatrics, Gifu University School of Medicine, Gifu, Gifu, 500, Japan;cLaboratory of Anatomy and Biology, Osaka Medical College, Daigaku-cho, Takatsuki, Osaka, 569, Japan;dLaboratory of Gene Structure I, Kazusa DNA Research Institute, Yana-Uchino, Kisarazu, Chiba, 292, Japan
Abstract:Chromosomal locations of theAtm(ataxia–telangiectasia (AT)-mutated) andAcat1(mitochondrial acetoacetyl-CoA thiolase) genes in mouse, rat, and Syrian hamster were determined by direct R-banding FISH. Both genes were colocalized to the C-D band of mouse chromosome 9, the proximal end of q24.1 of rat chromosome 8, and qa4–qa5 of Syrian hamster chromosome 12. The regions in the mouse and rat were homologous to human chromosome 11q. Fine genetic linkage mapping of the mouse AT region was performed using the interspecific backcross mice.Atm, Acat1,andNpat,which is a new gene isolated from the AT region, and 12 flanking microsatellite DNA markers were examined. No recombinations were found among theAtm, Npat, Acat1,andD9Mit6loci, and these loci were mapped 2.0 cM distal toD9Mit99and 1.3 cM proximal toD9Mit102.Comparison of the linkage map of mouse chromosome 9 (MMU9) and that of human chromosome 11 (HSA11) indicates that there is a chromosomal rearrangement due to an inversion betweenEts1andAtm–Npat–Acat1and that the inversion of MMU9 originated from the chromosomal breakage at the boundary betweenGria4andAtm–Npat–Acat1on HSA11. This type of inversion appeared to be conserved in the three rodent species, mouse, rat, and Syrian hamster, using additional comparative mapping data with theRckgene.
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