ArticleDNA and cell biology2016
Gen1 and Eme1 Play Redundant Roles in DNA Repair and Meiotic Recombination in Mice.
Article in DNA and cell biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 23 citations in OpenAlex.
- Association analysis of germline variants in GEN1 with a susceptibility to prostate cancer in Polish men.Hereditary cancer in clinical practice · 2026Article
- Analysis ofInternational journal of molecular sciences · 2025Article
- GEN1 as a risk factor for human congenital anomalies of the kidney and urinary tract.Human genomics · 2024Article
- Germline genetic biomarkers to stratify patients for personalized radiation treatment.Journal of translational medicine · 2022Article
- Intrauterine Low-Protein Diet Exacerbates Abnormal Development of the Urinary System inKidney diseases (Basel, Switzerland) · 2021Article
- Review
- Mechanisms of Genome Maintenance in Plants: Playing It Safe With Breaks and Bumps.Frontiers in genetics · 2021Review
- The Last Chance Saloon.Frontiers in cell and developmental biology · 2021Review
- Genetic evidence for the involvement of mismatch repair proteins, PMS2 and MLH3, in a late step of homologous recombination.The Journal of biological chemistry · 2020Article
- Article
- LEM-3 is a midbody-tethered DNA nuclease that resolves chromatin bridges during late mitosis.Nature communications · 2018Article
- Disruption ofInternational journal of biological sciences · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Resolution of the Holliday junction (HJ) is essential for homologous recombination and DNA repair. In Saccharomyces cerevisiae, HJ resolvase Yen1 and the Mus81-Mms4 complex are redundant in DNA damage repair. In cultured mammalian cells, such redundancy also exists between Yen1 ortholog GEN1 and the Mus81-Mms1 ortholog MUS81-EME1. In this report, we further tested if GEN1 and EME1 redundantly affect HJ-related physiological processes in mice. We found that combined homozygous mutations of Gen1 and Eme1 led to synthetic lethality during early embryonic stages. Homozygous Gen1 mutations did not cause DNA repair deficiency in mouse embryonic fibroblast (MEF) cells, but made heterozygous Eme1 mutant MEFs more sensitive to various DNA-damaging reagents. Gen1 mutations also reduced the meiotic recombination efficiency in Eme1 mutant mice. These results suggest that Gen1 and Eme1 play redundant roles in DNA repair and meiotic recombination in vivo.
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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.