Table of Contents
To view the fulltext, log-in or choose pay-per-view options:
Get Access

Nondisjunction in trisomy 21: Origin and mechanisms

Petersen M.B.a,b · Mikkelsen M.b
aDepartment of Genetics, Institute of Child Health, Athens (Greece); bDepartment of Medical Genetics, The John F. Kennedy Institute, Glostrup (Denmark) Cytogenet Cell Genet 91:199–203 (2000) (DOI:10.1159/000056844)

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.   

 

Individual Users: Register with Karger Login Information

Please create your User ID & Password





Contact Information











I have read the Karger Terms and Conditions and agree.


Pay-per-View Options
Direct payment This item at the regular price: USD 38.00
Payment from account With a Karger Pay-per-View account (down payment USD 150) you profit from a special rate for this and other single items.
This item at the discounted price: USD 26.50