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Chromosomal aneuploidy is the most frequent genetic damage observed in newborn children and originates as a rule from nondisjunction during maternal or paternal germ cell development. The error of chromosome segregation could be allocated in the past--at least in cases of 47,XXY--to maternal meiosis I (50%) or meiosis II (10%) and to paternal meiosis I (40%). Recent cytological improvements with various banding techniques enabled a further study on the origin of nondisjunction. Summarizing the published data one can argue that errors in Downs' syndrome are most often due to cleavage errors during maternal meiosis I. Approximately 70% of errors occur in oogenesis and only 30% in spermatogenesis. Maternal meiosis I seems also to be involved in most cases of fetal trisomy 16. Such a preferential missegregation of chromosomes offers the possibility of studying more closely the very mechanisms of nondisjunction in mammalian meiosis and early cleavages.

Clustering of chromosomal aneuploidy and tracing of nondisjunction in man.