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New Insights into Human Nondisjunction of Chromosome 21 in OocytesAuthor SummaryNondisjunction occurs when chromosomes fail to segregate during meiosis; when this happens, gametes with an abnormal number of chromosomes are produced. The clinical significance is high: nondisjunction is the leading cause of pregnancy loss and birth defects. We have studied trisomy 21 using DNA from individuals with Down syndrome and their parents to identify mechanisms underlying nondisjunction. The results from these studies show that altered patterns of recombination, e.g., no exchange, a single telomeric exchange and a single pericentromeric exchange, were associated with nondisjunction of chromosome 21 within the oocyte. In this report, we stratified maternal cases of trisomy 21 by the type of nondisjunction error (meiosis I or meiosis II) and by maternal age (ages <29, 29–34 and >34 years) and examined both the number and location of recombination by age group. Our results suggest that the risk imposed by the absence of exchange or by a single telomeric exchange is the same, irrespective of the age of the oocyte. In contrast, the risk imposed by a single pericentromeric exchange increases with increasing maternal age. These findings, put into the context of proteins involved in the meiotic process, have enabled us to further understand mechanisms underlying nondisjunction.
