ArticleMolecular and cellular biology2003
Replication and expansion of trinucleotide repeats in yeast.
Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
92 citing papers in PubMed, 164 citations in OpenAlex.
- Emerging drivers of DNA repeat expansions.Biochemical Society transactions · 2025Review
- The DNA replication checkpoint targets the kinetochore to reposition DNA structure-induced replication damage to the nuclear periphery.Cell reports · 2025Article
- Fast and accurate quantification of double-strand breaks in microsatellites by digital PCR.Biology methods & protocols · 2025Article
- Pathogenic CANVAS (AAGGG)n repeats stall DNA replication due to the formation of alternative DNA structures.Nucleic acids research · 2024Article
- A comparative cytogenetic study ofComparative cytogenetics · 2023Article
- Article
- The mechanism of replication stalling and recovery within repetitive DNA.Nature communications · 2022Article
- Rad9-mediated checkpoint activation is responsible for elevated expansions of GAA repeats in CST-deficient yeast.Genetics · 2021Article
- Restarted replication forks are error-prone and cause CAG repeat expansions and contractions.PLoS genetics · 2021Article
- Transcription-Replication Collisions-A Series of Unfortunate Events.Biomolecules · 2021Review
- Review
- Alternative DNA StructuresMicrobiology and molecular biology reviews : MMBR · 2021Review
- Common Threads: Aphidicolin-Inducible and Folate-Sensitive Fragile Sites in the Human Genome.Frontiers in genetics · 2021Review
- Gynecological Cancers Caused by Deficient Mismatch Repair and Microsatellite Instability.Cancers · 2020Review
- Resection and repair of a Cas9 double-strand break at CTG trinucleotide repeats induces local and extensive chromosomal deletions.PLoS genetics · 2020Article
- On the wrong DNA track: Molecular mechanisms of repeat-mediated genome instability.The Journal of biological chemistry · 2020Review
- The nuclear pore complex prevents sister chromatid recombination during replicative senescence.Nature communications · 2020Article
- Mrc1 and Tof1 prevent fragility and instability at long CAG repeats by their fork stabilizing function.Nucleic acids research · 2019Article
- Review
- Detours to Replication: Functions of Specialized DNA Polymerases during Oncogene-induced Replication Stress.International journal of molecular sciences · 2018Review
32 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The mechanisms of trinucleotide repeat expansions, underlying more than a dozen hereditary neurological disorders, are yet to be understood. Here we looked at the replication of (CGG)(n) x (CCG)(n) and (CAG)(n) x (CTG)(n) repeats and their propensity to expand in Saccharomyces cerevisiae. Using electrophoretic analysis of replication intermediates, we found that (CGG)(n) x (CCG)(n) repeats significantly attenuate replication fork progression. Replication inhibition for this sequence becomes evident at as few as approximately 10 repeats and reaches a maximal level at 30 to 40 repeats. This is the first direct demonstration of replication attenuation by a triplet repeat in a eukaryotic system in vivo. For (CAG)(n) x (CTG)(n) repeats, on the contrary, there is only a marginal replication inhibition even at 80 repeats. The propensity of trinucleotide repeats to expand was evaluated in a parallel genetic study. In wild-type cells, expansions of (CGG)(25) x (CCG)(25) and (CAG)(25) x (CTG)(25) repeat tracts occurred with similar low rates. A mutation in the large subunit of the replicative replication factor C complex (rfc1-1) increased the expansion rate for the (CGG)(25) repeat approximately 50-fold but had a much smaller effect on the expansion of the (CTG)(25) repeat. These data show dramatic sequence-specific expansion effects due to a mutation in the lagging strand DNA synthesis machinery. Together, the results of this study suggest that expansions are likely to result when the replication fork attempts to escape from the stall site.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.