Journal
CYTOGENETIC AND GENOME RESEARCH
Volume 100, Issue 1-4, Pages 7-24Publisher
KARGER
DOI: 10.1159/000072836
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Funding
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM063066] Funding Source: NIH RePORTER
- NIGMS NIH HHS [R01 GM063066, GM63066] Funding Source: Medline
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The trinucleotide repeats that expand to cause human disease form hairpin structures in vitro that are proposed to be the major source of their genetic instability in vivo. If a replication fork is a train speeding along a track of double-stranded DNA, the trinucleotide repeats are a hairpin curve in the track. Experiments have demonstrated that the train can become derailed at the hairpin curve, resulting in significant damage to the track. Repair of the track often results in contractions and expansions of track length. In this review we introduce the in vitro evidence for why CTG/CAG and CCG/CGG repeats are inherently unstable and discuss how experiments in model organisms have implicated the replication, recombination and repair machinery as contributors to trinuclecitide repeat instability in vivo. Copyright (C) 2002 S. Karger AG, Basel.
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