In the backcross progeny of single (Robertsonian) metacentric heterozygotes of the mouse, segregational impairment of fertility and reduced litter size are initiated by misdivision of trivalents in meiotic anaphase I. Males heterozygous for the metacentrics Rbl, Rb4, Rb5, and Rb7Bnr of the tobacco mouse series and for the Rb8–10Bnr metacentrics derived from other feral domestic mice produce variable rates of meiotic malsegregation, ranging from 4 to 26 unbalanced M II figures. Chromosomally unbalanced gametes become involved in fertilization and produce aneusomic zygotes. Fetal aneuploidy causes developmental breakdown and prenatal death. Mono-somic zygotes are eliminated at an early stage of development. Most aneuploid embryos observed beyond day 8 or 10 of gestation were trisomics. Aneuploidy (trisomy) of the zygotes was considerably more frequent in the progeny of heterozygous females than in that of heterozygous males. There was evidence that this disparity might be the result of a higher nondisjunction rate in the female gametogenesis. Mechanisms of selection against unbalanced male germ cells might operate on a small scale. The highest incidences of aneuploid implants were found (with decreasing frequencies) in the backcross progeny of the Rb(1.3)l, Rb(16.17)7, and Rb(11.13)4Bnr female heterozygotes. With the experimental design used in this study, several trisomic conditions could be observed and their phenotype and developmental profiles described, namely, trisomies (Ts) 1, 3, 4, 10, 11, 12, 13, 16, and 17. Among these, Ts 3, 11, and 17 were characterized by severe developmental impairment and relatively early death, whereas the others could survive until day 13 to 15 or, as in the case of Ts 12, even until day 17. Ts 1 displayed a syndrome of general hypoplasia (fetal runting), whereas exencephaly was found in Ts 12. It was the only trisomy observed in this study that was associated with gross malformatio
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