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Article

Chromosome fragility at GAA tracts in yeast depends on repeat orientation and requires mismatch repair.

The EMBO journal - 5 Nov 2008

Kim Hyun-Min, Narayanan Vidhya, Mieczkowski Piotr A, Petes Thomas D, Krasilnikova Maria M, Mirkin Sergei M, Lobachev Kirill S

Abstract excerpt

Expansion of triplex-forming GAA/TTC repeats in the first intron of FXN gene results in Friedreich's ataxia. Besides FXN, there are a number of other polymorphic GAA/TTC loci in the human genome where the size variations thus far have been considered to be a neutral event. Using yeast as a model system, we demonstrate that expanded GAA/TTC repeats represent a threat to eukaryotic genome integrity by triggering...

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Share to Chromosome Breakage
Share to Chromosome Fragility

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to DNA Mismatch Repair

Share to DNA Replication

Share to Gene Rearrangement

Share to Genes, Fungal

Share to Recombination, Genetic

Share to Repetitive Sequences, Nucleic Acid

Source

Open in PubMed Open full text

Identifiers

PMID: 18833189
DOI: 10.1038/emboj.2008.205
PMCID: PMC2580784

Genes

GAA
FXN

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

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Research trail→

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Chromosome fragility at GAA tracts in yeast depends on repeat orientation and requires mismatch repair.PMID 18833189Read ↗

Genome-wide screen identifies pathways that govern GAA/TTC repeat fragility and expansions in dividing and nondividing yeast cells.Semantic proximity Read ↗

Mutations in yeast replication proteins that increase CAG/CTG expansions also increase repeat fragility.Semantic proximity Read ↗

GAA instability in Friedreich's Ataxia shares a common, DNA-directed and intraallelic mechanism with other trinucleotide diseases.Semantic proximity Read ↗

Replication-independent instability of Friedreich's ataxia GAA repeats during chronological aging.Semantic proximity Read ↗

The Startling Role of Mismatch Repair in Trinucleotide Repeat Expansions.Semantic proximity Read ↗

Dynamic mutations: a decade of unstable expanded repeats in human genetic disease.Semantic proximity Read ↗

Large-scale contractions of Friedreich's ataxia GAA repeats in yeast occur during DNA replication due to their triplex-forming ability.Semantic proximity Read ↗

Large-scale expansions of Friedreich’s ataxia GAA•TTC repeats in human cells are prevented by LNA-DNA oligonucleotides and PNA oligomersSemantic proximity Read ↗

Cruciform-forming AT/TA repeats are acted upon by structure selective endonucleases and Rad51 prior to repositioning to the nuclear periphery for repairSemantic proximity Read ↗

Large-scale expansions and replication stalling of Friedreich’s ataxia GAA repeats in an experimental mammalian systemSemantic proximity Read ↗

Trinucleotide instability: a repeating theme in human inherited disorders.Semantic proximity Read ↗

The stabilization of repetitive tracts of DNA by variant repeats requires a functional DNA mismatch repair system.Semantic proximity Read ↗

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