ArticleMolecular and cellular biology1999
Stability of the human fragile X (CGG)(n) triplet repeat array in Saccharomyces cerevisiae deficient in aspects of DNA metabolism.
Article in Molecular and cellular biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
35 citing papers in PubMed, 95 citations in OpenAlex.
- The polyG diseases: a new disease entity.Acta neuropathologica communications · 2022Review
- Molecular Pathogenesis and Peripheral Monitoring of Adult Fragile X-Associated Syndromes.International journal of molecular sciences · 2021Review
- On the wrong DNA track: Molecular mechanisms of repeat-mediated genome instability.The Journal of biological chemistry · 2020Review
- Large-scale contractions of Friedreich's ataxia GAA repeats in yeast occur during DNA replication due to their triplex-forming ability.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Review
- DNA Replication Dynamics of the GGGGCC Repeat of the C9orf72 Gene.The Journal of biological chemistry · 2015Article
- The balancing act of DNA repeat expansions.Current opinion in genetics & development · 2013Review
- The role of DNA exonucleases in protecting genome stability and their impact on ageing.Age (Dordrecht, Netherlands) · 2012Review
- DNA base excision repair: a mechanism of trinucleotide repeat expansion.Trends in biochemical sciences · 2012Review
- Complementary roles for exonuclease 1 and Flap endonuclease 1 in maintenance of triplet repeats.The Journal of biological chemistry · 2010Article
- Potassium bromate, a potent DNA oxidizing agent, exacerbates germline repeat expansion in a fragile X premutation mouse model.Human mutation · 2010Article
- Coordination between polymerase beta and FEN1 can modulate CAG repeat expansion.The Journal of biological chemistry · 2009Article
- FMR1: a gene with three faces.Biochimica et biophysica acta · 2009Review
- Comparative genomics and molecular dynamics of DNA repeats in eukaryotes.Microbiology and molecular biology reviews : MMBR · 2008Review
- Rapid unwinding of triplet repeat hairpins by Srs2 helicase of Saccharomyces cerevisiae.Nucleic acids research · 2008Article
- ATR protects the genome against CGG.CCG-repeat expansion in Fragile X premutation mice.Nucleic acids research · 2008Article
- Replication fork stalling at natural impediments.Microbiology and molecular biology reviews : MMBR · 2007Review
- An origin of DNA replication in the promoter region of the human fragile X mental retardation (FMR1) gene.Molecular and cellular biology · 2007Article
- Role of replication and CpG methylation in fragile X syndrome CGG deletions in primate cells.American journal of human genetics · 2005Article
- Mechanistic features of CAG*CTG repeat contractions in cultured cells revealed by a novel genetic assay.Nucleic acids research · 2005Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Expanded trinucleotide repeats underlie a growing number of human diseases. The human FMR1 (CGG)(n) array can exhibit genetic instability characterized by progressive expansion over several generations leading to gene silencing and the development of the fragile X syndrome. While expansion is dependent upon the length of uninterrupted (CGG)(n), instability occurs in a limited germ line and early developmental window, suggesting that lineage-specific expression of other factors determines the cellular environment permissive for expansion. To identify these factors, we have established normal- and premutation-length human FMR1 (CGG)(n) arrays in the yeast Saccharomyces cerevisiae and assessed the frequency of length changes greater than 5 triplets in cells deficient in various DNA repair and replication functions. In contrast to previous studies with Escherichia coli, we observed a low frequency of orientation-dependent large expansions in arrays carrying long uninterrupted (CGG)(n) arrays in a wild-type background. This frequency was unaffected by deletion of several DNA mismatch repair genes or deletion of the EXO1 and DIN7 genes and was not enhanced through meiosis in a wild-type background. Array contraction occurred in an orientation-dependent manner in most mutant backgrounds, but loss of the Sgs1p resulted in a generalized increase in array stability in both orientations. In contrast, FMR1 arrays had a 10-fold-elevated frequency of expansion in a rad27 background, providing evidence for a role in lagging-strand Okazaki fragment processing in (CGG)(n) triplet repeat expansion.
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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.