A sample of 100 trisomy 18 conceptuses analysed separately and togethe
r with a published sample of 61 conceptuses confirms that an error in
maternal meiosis II (MII) is the most frequent cause of nondisjunction
for chromosome 18, This is unlike all other human trisomies that have
been studied, which show a higher frequency in maternal meiosis I (MI
), Maternal MI trisomy 18 shows a low frequency of recombination in pr
oximal p and medial q, but not the reduction in proximal q observed in
chromosome 21 MI non-disjunction, Maternal MII non-disjunction does n
ot fit the entanglement model that predicts increased recombination, e
specially near the centromere, Whereas recent data on MII trisomy 21 s
how the predicted increase in recombination proximally, maternal MII t
risomy 18 has non-significantly reduced recombination. Therefore, chro
mosome-specific factors must complicate the simple model of susceptibl
e chiasma distributions interacting with age-dependent deterioration o
f the meiotic mechanism, For chromosome 18, 30% of tetrads are nullich
iasmate in maternal MI non-disjunction, but nullichiasmates are not ob
served in maternal MII non-disjunction. Chiasma distributions from nor
mal chromosome 18 meioses provide no evidence for normal disjunction f
rom nullichiasmate tetrads, We extend this study to examine the remain
ing autosomes and find no evidence for normal disjunction from nullich
iasmate tetrads generally.