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The Journal of Heredity 2001:92(4)
© 2001 The American Genetic Association 92:352-355

Brief Communication

Unique Mutations in Mitochondrial DNA of Senescence-Accelerated Mouse (SAM) Strains

J. Mizutani, T. Chiba, M. Tanaka, K. Higuchi, and M. Mori

From the Department of Aging Angiology, Research Center on Aging and Adaptation, Shinshu University School of Medicine, 3-1-1 Asahi, Matsumoto 390-8621, Japan (Mizutani, Chiba, Higuchi, and Mori), and Department of Gene Therapy, Gifu International Institute of Biotechnology, Yagi Memorial Park, Nataki, Gifu, Japan (Tanaka).

Address correspondence to Masayuki Mori, Ph.D. at the address above or e-mail: masamori{at}sch.md.shinshu-u.ac.jp

Mitochondrial DNA (mtDNA) is exclusively inherited maternally and hence could offer a good method for tracing the lineage of mouse strains. We examined the mtDNA sequence of senescence-accelerated mouse (SAM) strains as well as other laboratory strains of inbred mice to deduce the ancestral strain of SAM. Four unique mutations were identified at bases 2256, 10,847, 11,181, and 13,053 in SAM strains. The mutations were not found in other mouse strains including AKR/J, one of the parental strains of SAM. Comparison of the mtDNA sequences also led to the consensus mtDNA sequence of laboratory strains of inbred mice. The seven laboratory strains of common inbred mice showed polymorphisms at base 9348, thymine repeat from base 9818, and adenine repeat from base 9821, and could be classified into five types by combination of the differences. Although we could not identify mouse strains with the same type of mtDNA as SAM in this study, the polymorphisms would provide a promising clue to ascertain the ancestral strain(s) of SAM. The polymorphism in mtDNA could be used to ascertain the genealogy of other mouse strains as well.


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