ArticleGenetics2001
Overlapping functions of the Saccharomyces cerevisiae Mre11, Exo1 and Rad27 nucleases in DNA metabolism.
Article in Genetics, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 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
101 citing papers in PubMed, 172 citations in OpenAlex.
- Activation of Pol theta-mediated end joining begins during mitotic commitment.bioRxiv : the preprint server for biology · 2026Article
- Role of chromatin remodeling and immunopharmacology in cancer therapy.Molecular medicine (Cambridge, Mass.) · 2026Review
- Asymmetrical recognition and processing of double-strand breaks formed during DNA replication.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Cohesin reconstitution and homologous recombination repair of DNA double-strand breaks in late mitosis.eLife · 2025Article
- S-phase checkpoint protects from aberrant replication fork processing and degradation.Nucleic acids research · 2025Article
- The Slx4-Rad1-Rad10 nuclease differentially regulates deletions and duplications induced by a replication fork barrier.PLoS genetics · 2025Article
- Article
- Article
- A Role for the Mre11-Rad50-Xrs2 Complex in Gene Expression and Chromosome Organization.Molecular cell · 2021Article
- Mutation of Conserved Mre11 Residues Alter Protein Dynamics to Separate Nuclease Functions.Journal of molecular biology · 2020Article
- Tel1 Activation by the MRX Complex Is Sufficient for Telomere Length Regulation but Not for the DNA Damage Response inGenetics · 2019Article
- Human Exonuclease 1 (EXO1) Regulatory Functions in DNA Replication with Putative Roles in Cancer.International journal of molecular sciences · 2018Review
- Review
- Physiological protein blocks direct the Mre11-Rad50-Xrs2 and Sae2 nuclease complex to initiate DNA end resection.Genes & development · 2017Article
- Checkpoint Kinase Rad53 Couples Leading- and Lagging-Strand DNA Synthesis under Replication Stress.Molecular cell · 2017Article
- Recombination at subtelomeres is regulated by physical distance, double-strand break resection and chromatin status.The EMBO journal · 2017Article
- Homologous recombination in budding yeast expressing the human RAD52 gene reveals a Rad51-independent mechanism of conservative double-strand break repair.Nucleic acids research · 2017Article
- Article
- Small molecule inhibitors uncover synthetic genetic interactions of human flap endonuclease 1 (FEN1) with DNA damage response genes.PloS one · 2017Article
- Consider the workhorse: Nonhomologous end-joining in budding yeast.Biochemistry and cell biology = Biochimie et biologie cellulaire · 2016Review
41 more citing papers are in PubMed but not listed here.
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 1 institution in 1 country.
Funding
Abstract
MRE11 functions in several aspects of DNA metabolism, including meiotic recombination, double-strand break repair, and telomere maintenance. Although the purified protein exhibits 3' to 5' exonuclease and endonuclease activities in vitro, Mre11 is implicated in the 5' to 3' resection of duplex ends in vivo. The mre11-H125N mutation, which eliminates the nuclease activities of Mre11, causes an accumulation of unprocessed double-strand breaks (DSBs) in meiosis, but no defect in processing HO-induced DSBs in mitotic cells, suggesting the existence of redundant activities. Mutation of EXO1, which encodes a 5' to 3' exonuclease, was found to increase the ionizing radiation sensitivity of both mre11Delta and mre11-H125N strains, but the exo1 mre11-H125N strain showed normal kinetics of mating-type switching and was more radiation resistant than the mre11Delta strain. This suggests that other nucleases can compensate for loss of the Exo1 and Mre11 nucleases, but not of the Mre11-Rad50-Xrs2 complex. Deletion of RAD27, which encodes a flap endonuclease, causes inviability in mre11 strains. When mre11-H125N was combined with the leaky rad27-6, the double mutants were viable and no more gamma-ray sensitive than the mre11-H125N strain. This suggests that the double mutant defect is unlikely to be due to defective DSB processing.
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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.