Spontaneous heteroploidy in one-cell mouse embryos

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.

The murine Rb(6.16) translocation: evidence for sperm selection and a modulating effect of aging

“…The two hyperhaploid sperm, one seen in each of the mating groups, gave a frequency of 0.65%. This incidence is less than the 0.93% seen in our laboratory for the outbred Swiss mouse (Martin-DeLeon and Boice 1983) and indicates that the translocation did not disrupt normal pairing and disjunction of homologues. Thus, this study provides no evidence for an interchromosomal effect for carriers of a single Robertsonian translocation, and corroborates the finding reported in human translocation carriers (Pellestor 1990).…”

Aneuploidy in the embryonic progeny of females heterozygous for the Robertsonian chromosome (9.12) in genetically wild Peru--Coppock mice (Mus musculus)

“…In the same study, however, other metacentric combinations did not yield such relatively high triploid frequencies. In normal matings in laboratory strains/stocks, frequencies of 0-4% spontaneous triploidy in one-cell embryos have been reported (see Martin-DeLeon & Boice, 1983, for references), but their subsequent fate appears to depend on genetic background (Wroblewska, 1971). Although some triploids may survive to the stage of organogénesis (Fischberg & Beatty, 1951) and appear structurally normal up to 11^d ays of gestation (Vickers, 1969), many show a characteristic disturbance in embryogenesis at Day 9 (Wroblewska, 1971) or severe retardation at Day 9 as observed in our study.…”

Analyses of Developmental Ability of (BALB/c*C57BL/6) F1 and ICR Mouse Embryos Fertilized In Vitro and Their Chromosome at the First Cleavage Division.

“…The incidences of structural aberrations in F1 and ICR mouse eggs are within the range 0.9 to 2.2% reported in mouse eggs fertilized in vitro [15,20,22] and that (0.4 to 2.2%) in mouse eggs fertilized in vivo [15,27,30,31].…”

“…Concerning the primary sex ratio examined at the first cleavage stage by means of chromosomal sexing, the values so far reported range from 43 to 55% males [15,27,[31][32][33], but no statistically significant deviation from equality has been observed in most of the cases. Similarly the lower sex ratios in both F1 and ICR eggs were not of statistical significance.…”