One observation, however, deserves particular attention. Indeed, in the 0.4 Gy group, we found a litter where all 13 fetuses carried both postaxial and preaxial polydactyly, with either 3 of 4 limbs affected. Postaxial polydactyly was expressed in the forelimbs, while preaxial polydactyly was located in the hindlimbs. The genetic origin of such “crossed” polydactyly remains unknown. At least 26 mutant genes which produce polydactyly in mice are known, and 12 of them were reported to be dominant [21–27]. The phenotype of the 13 polydactylous fetuses that were found in the same litter strongly evokes that caused by the Nagoya domi. nant mutation Pdn in JCL:ICR mice [22]. Heterozygous Pdn/+ fetuses and newborn often have a tab on the postaxial side of the forelimb and one extra-digit on the preaxial side of the hindlimb. The tab of the forelimb regress and the extra-digit of the hindlimb becomes rudimentary when the mice grow up. Homozygotes for that dominant mutation are not viable and die either in utero or soon after birth.