Abstract

First cleavage divisions were analyzed, after chromosome banding, in 321 zygotes recovered from superovulated, outbred ICR mice 33-35 h after injection of human chorionic gonadotropin. With 72.1% of all zygotes at metaphase and late prophase analyzed, there was 87% diploidy, 3.6% trisomy, 2.5% monosomy, 0.4% structural rearrangement, and 0.93% triploidy. Aneuploid zygotes in which there were 37 or 38 chromosomes accounted for 6.5% of the population with both haploid complements analyzable. In 45 diploid zygotes in which only one complement was analyzable, there was 93.4% haploidy, 2.2% disomy, and 4.4% hypoploidy. The chromosome most often involved in aneuploidy was the 19. The parental origin of the chromosome anomalies was determined on the basis of differential condensation of the chromosomes. The source of trisomy was shown to be the male in three and the female in five of the eight cases determined. This indicates a paternal contribution to trisomy and a female nondisjunction frequency of 1.5% (five of 321). For monosomy where the origin was identified in five of the cases, the male complement was implicated in three zygotes. The single break was seen in a sperm-derived chromosome. Two of the three triploids were dispermic and one was digynic. The outbred Swiss mouse might be a useful model for studying factors responsible for the induction of cytogenetic anomalies in early development of mammals.

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