D. Warburton et A. Kinney, CHROMOSOMAL DIFFERENCES IN SUSCEPTIBILITY TO MEIOTIC ANEUPLOIDY, Environmental and molecular mutagenesis, 28(3), 1996, pp. 237-247
A basic question concerning the origins of germ cell aneuploidy is whe
ther the same mechanisms operate for all chromosomes, or whether there
are chromosome-specific factors influencing the susceptibility to non
disjunction. Although selective loss of some trisomies in early gestat
ion may contribute to the observed differences in trisomy frequency, d
ata from spontaneous abortions, early embryos and gametes strongly sug
gest that there are real differences in the frequency with which diffe
rent trisomies arise. In particular the preponderance of trisomy 16 an
d acrocentric trisomy appears to be present at conception. Maternal an
d paternal age relationships also differ among trisomies, as do the ex
tent of maternal and paternal contributions, and the relative frequenc
y of meiosis I and meiosis II errors. Recombination patterns associate
d with nondisjunction also show chromosomal differences. Chromosomal d
ifferences in length, centromere position, pericentromeric and other r
epetitive sequences, recombination patterns and chromatin characterist
ics might all be related to a differential susceptibility to aneuploid
y, but no current explanation accounts for the excess of maternally de
rived trisomy 16. The existence of chromosome-specific factors makes e
xtrapolation from observations on one chromosome to all aneuploidy unw
ise, both for investigations into the causes of aneuploidy, and for su
rveillance of aneuploidy frequency. (C) 1996 Wiley-Liss, Inc.