Genetic analysis of lifespan in hybrid progeny derived from the SAMP1 mouse strain with accelerated senescence

Abstract

The SAMP1 mouse, a senescence-accelerated mouse prone (SAMP) strain, shows accelerated senescence coupled with a short lifespan as a genetic trait, and has been used in gerontological research. The accelerated senescence and short lifespan of SAMP strains is considered to be under the control of multiple genes. To identify the chromosomal regions encompassing the genes for the accelerated senescence and short lifespan, we performed whole genome scanning with polymorphic marker loci in a progeny from a cross between the SAMP1 strain and normal B10.BR strain. A genetically recessive effect of the amyloidogenic Apoa2(c) allele from SAMP1 on chromosome 1 to shorten the lifespan was demonstrated in the progeny, consistent with the previous report. The recessive effect was observed also at D1Mit67, D5Mit267, D6Mit384 and D19Mit33, suggesting the presence of genes for accelerated senescence in the SAMP strains around these loci. Other markers on chromosomes 8, 14, 16, and 17, however, exhibited a dominant or additive effect to shorten or prolong the lifespan, demonstrating a complex genetic control of the trait.