Genetic typing of the Senescence-Accelerated Mouse (SAM) strains with microsatellite markers |
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Authors: | Chen Xia Keiichi Higuchi Motoyuki Shimizu Takatoshi Matsushita Kumiko Kogishi Jing Wang Takuya Chiba Michael FW Festing Masanori Hosokawa |
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Institution: | (1) Field of Regeneration Control, Institute for Frontier Medical Sciences, Kyoto University, Sakyo-ku, Kyoto 606-8397, Japan, JP;(2) Department of Aging Angiology, Research Center on Aging and Adaptation, Shinshu University School of Medicine, Asahi, Matsumoto, 390-8621, Japan, JP;(3) Department of Orthopedic Surgery, Faculty of Medicine, Kyoto University, Sakyo-ku, Kyoto 606-8397, Japan, JP;(4) MRC Toxicology Unit, University of Leicester, P.O. Box 138, Lancaster Road, Leicester LE1 9HN, UK, GB |
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Abstract: | The Senescence-Accelerated Mouse (SAM) strains constitute a murine model of accelerated senescence originating from the ancestral
AKR/J strains and consist of nine senescence-prone (SAMP) strains and four senescence-resistant (SAMR) strains. The chromosomes
(Chrs) of the SAM strains were typed with 581 microsatellite markers amplified by PCR, and the fundamental genetic information
of the SAM strains was obtained. One-third of the examined markers displayed polymorphism among the strains, and only two
alleles were detected in almost all loci among the SAM and AKR/J strains. However, in 12 loci (5.6% of total 215 polymorphic
markers), the third allele was detected among the SAM strains. The genetic typing and developmental history suggested that
the SAM strains were related inbred strains developed by the accidental crossing between the AKR/J strain and other unknown
strain(s). Comparison of the distribution of the loci in the SAMP and the SAMR series revealed notable differences in the
four regions on Chrs 4, 14, 16, and 17. This indicated that some of these chromosomal sites might contain the genes responsible
for accelerated senescence in the SAMP series.
Received: 17 July 1998 / Accepted: 17 November 1998 |
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