ArticleGenetics1999
The effect of DNA replication mutations on CAG tract stability in yeast.
Article in Genetics, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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.
The trial behind it
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
31 citing papers in PubMed, 66 citations in OpenAlex.
- Restarted replication forks are error-prone and cause CAG repeat expansions and contractions.PLoS genetics · 2021Article
- Defects in the GINS complex increase the instability of repetitive sequences via a recombination-dependent mechanism.PLoS genetics · 2019Article
- Expansion of CAG repeats in Escherichia coli is controlled by single-strand DNA exonucleases of both polarities.Genetics · 2014Article
- Expression levels of DNA replication and repair genes predict regional somatic repeat instability in the brain but are not altered by polyglutamine disease protein expression or age.Human molecular genetics · 2014Article
- Article
- The balancing act of DNA repeat expansions.Current opinion in genetics & development · 2013Review
- Role of DNA polymerases in repeat-mediated genome instability.Cell reports · 2012Article
- Instability of (CTG)n•(CAG)n trinucleotide repeats and DNA synthesis.Cell & bioscience · 2012Article
- Mechanisms of trinucleotide repeat instability during human development.Nature reviews. Genetics · 2010Review
- The Rtt109 histone acetyltransferase facilitates error-free replication to prevent CAG/CTG repeat contractions.DNA repair · 2010Article
- Article
- CTG/CAG repeat instability is modulated by the levels of human DNA ligase I and its interaction with proliferating cell nuclear antigen: a distinction between replication and slipped-DNA repair.The Journal of biological chemistry · 2009Article
- Article
- Suppression of a DNA polymerase delta mutation by the absence of the high mobility group protein Hmo1 in Saccharomyces cerevisiae.Current genetics · 2009Article
- Checkpoint responses to unusual structures formed by DNA repeats.Molecular carcinogenesis · 2009Review
- Comparative genomics and molecular dynamics of DNA repeats in eukaryotes.Microbiology and molecular biology reviews : MMBR · 2008Review
- Article
- Hijacking of the mismatch repair system to cause CAG expansion and cell death in neurodegenerative disease.DNA repair · 2008Review
- Article
- Replication fork stalling at natural impediments.Microbiology and molecular biology reviews : MMBR · 2007Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
CAG repeat tracts are unstable in yeast, leading to frequent contractions and infrequent expansions in repeat tract length. To compare CAG repeats to other simple repeats and palindromic sequences, we examined the effect of DNA replication mutations, including alleles of pol alpha, pol delta, pol epsilon, and PCNA (proliferating cell nuclear antigen), on tract stability. Among the polymerase mutations, the pol delta mutation (pol3-14) destabilizes tracts with either CAG or CTG as the lagging strand template. One pol alpha mutation, pol1-1, destabilizes the orientation with CAG as the lagging strand template, but it has little effect on the CTG orientation. In contrast, the pol1-17 mutation has no effect on either orientation. Similarly, mutations in the proofreading functions of pol delta and pol epsilon, as well as a temperature-sensitive pol epsilon mutation, pol2-18, have no effect on tract stability. Three PCNA mutations, pol30-52, pol30-79, and pol30-90, all have drastic effects on tract stability. Of the three, pol30-52 is unique in yielding small tract changes that are indicative of an impairment in mismatch repair. These results show that while CAG repeats are destabilized by many of the same mutations that destabilize other simple repeats, they also have some behaviors that are suggestive of their potential to form hairpin structures.
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What OpenQuestion holds
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.