ArticleMolecular and cellular biology2005
Novel PMS1 alleles preferentially affect the repair of primer strand loops during DNA replication.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- RIOK1: A Novel Oncogenic Driver in Hepatocellular Carcinoma.Cancer medicine · 2025Article
- CircPMS1 promotes proliferation of pulmonary artery smooth muscle cells, pulmonary microvascular endothelial cells, and pericytes under hypoxia.Animal models and experimental medicine · 2024Article
- Experimental exchange of paralogous domains in the MLH family provides evidence of sub-functionalization after gene duplication.G3 (Bethesda, Md.) · 2021Article
- Expanded roles for the MutL family of DNA mismatch repair proteins.Yeast (Chichester, England) · 2021Review
- High-throughput synthetic rescue for exhaustive characterization of suppressor mutations in human genes.Cellular and molecular life sciences : CMLS · 2020Review
- Absence of MutSβ leads to the formation of slipped-DNA for CTG/CAG contractions at primate replication forks.DNA repair · 2016Article
- Different roles of eukaryotic MutS and MutL complexes in repair of small insertion and deletion loops in yeast.PLoS genetics · 2013Article
- Yeast mutator phenotype enforced by Arabidopsis PMS1 expression.Molecular biology reports · 2013Article
- In vivo analysis in Drosophila reveals differential requirements of contact residues in Axin for interactions with GSK3beta or beta-catenin.Developmental biology · 2010Article
- Human postmeiotic segregation 2 exhibits biased repair at tetranucleotide microsatellite sequences.Cancer research · 2009Article
- Mutations affecting a putative MutLalpha endonuclease motif impact multiple mismatch repair functions.DNA repair · 2007Article
- The E705K mutation in hPMS2 exerts recessive, not dominant, effects on mismatch repair.Cancer letters · 2007Article
- DNA mismatch repair and Lynch syndrome.Journal of molecular histology · 2006Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Null mutations in DNA mismatch repair (MMR) genes elevate both base substitutions and insertions/deletions in simple sequence repeats. Data suggest that during replication of simple repeat sequences, polymerase slippage can generate single-strand loops on either the primer or template strand that are subsequently processed by the MMR machinery to prevent insertions and deletions, respectively. In the budding yeast Saccharomyces cerevisiae and mammalian cells, MMR appears to be more efficient at repairing mispairs comprised of loops on the template strand compared to loops on the primer strand. We identified two novel yeast pms1 alleles, pms1-G882E and pms1-H888R, which confer a strong defect in the repair of "primer strand" loops, while maintaining efficient repair of "template strand" loops. Furthermore, these alleles appear to affect equally the repair of 1-nucleotide primer strand loops during both leading- and lagging-strand replication. Interestingly, both pms1 mutants are proficient in the repair of 1-nucleotide loop mispairs in heteroduplex DNA generated during meiotic recombination. Our results suggest that the inherent inefficiency of primer strand loop repair is not simply a mismatch recognition problem but also involves Pms1 and other proteins that are presumed to function downstream of mismatch recognition, such as Mlh1. In addition, the findings reinforce the current view that during mutation avoidance, MMR is associated with the replication apparatus.
Indexed as
Identifiers
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.