A basic question concerning the origins of germ cell aneuploidy is whether the same mechanisms operate for all chromosomes, or whether there are chromosomespecific factors influencing the suscep tibility to nondisiunction. Although selective loss of some trisomies in early gestation may contribute to the observed differences in trisomy frequency, data from spontaneous abortions, early embryos and gametes strongly suggest that there are real differences in the frequency with which different trisomies arise. In particular the preponderance of trisomy 16 and acrocentric trisomy appears to be present at conception. Maternal and paternal age relationships also differ among trisomies, as do the extent of maternal and paternal contributions, and the rel-ative frequency of meiosis I and meiosis II errors.
Recombination patterns associated with nondisiunction also show chromosomal differences. Chromosomal differences in length, centromere position, pericentromeric and other repetitive sequences, r e combination patterns and chromatin characteristics might all be related to a differential susceptibility to aneuploidy, but no current explanation accounts for the excess of maternally derived trisomy 16. The existence of chromosome-specific factors makes extrapolation from observations on one chromosome to all aneuploidy unwise, both for investigations into the causes of aneuploidy, and for surveillance of aneuploidy frequency. o 1996 WiIey-Liss, Inc.