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Vol. 91, No. 1-4, 2000
Issue release date: 2000
Section title: Paper
Cytogenet Cell Genet 91:199–203 (2000)
(DOI:10.1159/000056844)

Nondisjunction in trisomy 21: Origin and mechanisms

Petersen M.B. · Mikkelsen M.
aDepartment of Genetics, Institute of Child Health, Athens (Greece); bDepartment of Medical Genetics, The John F. Kennedy Institute, Glostrup (Denmark)

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Article / Publication Details

First-Page Preview
Abstract of Paper

Published online: 1/30/2001

Number of Print Pages: 5
Number of Figures: 0
Number of Tables: 2

ISSN: 1424-8581 (Print)
eISSN: 1424-859X (Online)

For additional information: http://www.karger.com/CGR

Abstract

Chromosomal aneuploidy is a fundamental characteristic of the human species. In this review we summarize the knowledge about the origin and mechanisms of nondisjunction in human trisomy 21 that has accumulated during the last decade by using DNA polymorphism analysis. The first molecular correlate of nondisjunction in humans is altered recombination, meiosis I errors being associated with reduced recombination and maternal meiosis II errors with increased recombination between the nondisjoined chromosomes. Thus, virtually all maternal meiotic errors of chromosome 21 seem to be initiated in meiosis I. Advanced maternal age remains the only well documented risk factor for maternal meiotic nondisjunction, but there is, however, still a surprising lack of understanding of the basic mechanisms behind the maternal age effect.   


Article / Publication Details

First-Page Preview
Abstract of Paper

Published online: 1/30/2001

Number of Print Pages: 5
Number of Figures: 0
Number of Tables: 2

ISSN: 1424-8581 (Print)
eISSN: 1424-859X (Online)

For additional information: http://www.karger.com/CGR


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