Abstract
Asada et al. reported that EL/Sea (EL) mice having 97% incidence rates of absence of all of the third molars and showing no significant difference between sexes were useful models for studying the cause of the absence of the third molars. Nakamura et al. performed the genetic crosses using two strains of mice, EL with absence of the third molars and MSM/Msf (MSM) with the normal complement of teeth. It was suggested that the absence of the third molars in EL mice was strongly controlled by genetic factor(s), and was recessively influenced by autosomal genetic factors. The cause of this abnormality, however, was still unclear. The purpose of the present study was to identify the candidate chromosome and to detect the region that included causative gene(s) causing absence of the third molars in EL mice. To screen the linkages between candidate gene and DNA markers, in formative markers were selected from polymorphisms between EL and MSM. Over fifty selected markers Nomura et al. obtained were distributed throughout the autosomal genome. In the present study, all chromosomes were, therefore, examined by the individual genotyping of the 10 F 2 intercross mice [(EL×MSM)F1×F1] with absence of the third molars. In rough mapping, high linkage was obtained at D 3 Mit 141 (genotype ratio of EL homozygous: EL/MSM heterozygous: MSM homozygous 9: 0: 1, χ2=22.8, p<0.0001). Based on the results, there possibility was found that a candidate gene causing absence of the third molar might exist on chromosome 3. Therefore linkage analysis was performed in detail on chromosome 3. The gene causing absence of the third molars in EL mice was mapped in the region from D 3 Mit 125 to D 3 Mit 17 (genotype ratio 9: 1: 0, χ2=22.6, p<0.0001) and from D 3 Mit 141 to D 3 Mit 290 (genotype ratio 9: 0: 1, χ2=22.8, p<0.0001).
