International Mammalian Genome Society

The 14th International Mouse Genome Conference (2000)

Table of Contents * Genes, Physical Mapping and Sequencing * Gene Identification * Bioinformatics * Common Resources * RIKEN Session * Functional Genomics * Complex Traits * Mutagenesis * Developmental Genetics and Differentiation * Verne Chapman Memorial Lecture I and II

G10. Mapping of the Genes Responsible for the Performance in the Passive Avoidance Test Using Strains Derived from Wild Mice

Tsuyoshi Koide^1,4, Tamio Furuse^1,2, Kazuo Moriwaki³ and Toshihiko Shiroishi^1
1National Institute of Genetics, Mishima, Shizuoka-ken, 411-8540 Japan
² Tokyo University of Agriculture and Technology, Fuchuu, Tokyo
³Graduate University of Advanced Studies, Hayama, Kanagawa-ken
⁴PRESTO, Japan Science and Technology Corporation

Many aspects of mouse behavior have been studied using only a relatively small sample of available laboratory strains. An inherent problem in analyzing mouse behavior is that genetic diversity is limited among currently available strains. In this respect, the use of strains which are derived from a variety of wild mice should provide a means to identifying novel behavioral phenotypes. We previously invested several behavioral phenotypes using females of a number of mouse strains derived from wild mice of different subspecies, BFM/2, NJL, BLG2, HMI, CAST/Ei, KJR, SWN and MSM, a strain derived from fancy mice, JF1, and two laboratory strains, C57BL/6 and DBA/1. We reported that the two strains, CAST/Ei and BLG2, are the poor learners although five strains, BFM/2, KJR, SWN, MSM and C57BL/6, are the good learners in the passive avoidance test. In order to map the genes which are involved in the different performance between strains, we collected the progeny from three different crosses, (C57BL/6 x BLG2) x BLG2, (KJR x BLG2) x BLG2 and (SWN x BLG2) x BLG2. The performance in the passive avoidance test was analyzed in each mouse. The tail DNAs were prepared for the following genetic studies. The genome wide scanning using microsatellite markers were conducted using 94 mouse progeny from each cross. Linkage was observed on chromosomes 1 and 14 in the cross (C57BL/6 x BLG2) x BLG2. Further genetic mapping are currently underway.