ArticleThe EMBO journal1998
Saccharomyces cerevisiae LIF1: a function involved in DNA double-strand break repair related to mammalian XRCC4.
Article in The EMBO journal, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed.
- Unwrap RAP1's Mystery at Kinetoplastid Telomeres.Biomolecules · 2024Review
- Saccharomyces cerevisiae DNA polymerase IV overcomes Rad51 inhibition of DNA polymerase δ in Rad52-mediated direct-repeat recombination.Nucleic acids research · 2023Article
- Review
- Easy efficient HDR-based targeted knock-in inBioengineered · 2022Article
- Human DNA ligase IV is able to use NAD+ as an alternative adenylation donor for DNA ends ligation.Nucleic acids research · 2019Article
- Nonhomologous DNA end-joining for repair of DNA double-strand breaks.The Journal of biological chemistry · 2018Review
- Shepherding DNA ends: Rif1 protects telomeres and chromosome breaks.Microbial cell (Graz, Austria) · 2018Review
- Fumarase: From the TCA Cycle to DNA Damage Response and Tumor Suppression.Frontiers in molecular biosciences · 2018Review
- The non-homologous end-joining factor Nej1 inhibits resection mediated by Dna2-Sgs1 nuclease-helicase at DNA double strand breaks.The Journal of biological chemistry · 2017Article
- Efficient gene targeting in non-homologous end-joining-deficient Lipomyces starkeyi strains.Current genetics · 2017Article
- Non-homologous DNA end joining and alternative pathways to double-strand break repair.Nature reviews. Molecular cell biology · 2017Review
- Regulation of non-homologous end joining via post-translational modifications of components of the ligation step.Current genetics · 2017Review
- Development of a sufficient and effective procedure for transformation of an oleaginous yeast, Rhodosporidium toruloides DMKU3-TK16.Current genetics · 2017Article
- Consider the workhorse: Nonhomologous end-joining in budding yeast.Biochemistry and cell biology = Biochimie et biologie cellulaire · 2016Review
- The non-homologous end-joining pathway of S. cerevisiae works effectively in G1-phase cells, and religates cognate ends correctly and non-randomly.DNA repair · 2016Article
- New vectors for simple and streamlined CRISPR-Cas9 genome editing in Saccharomyces cerevisiae.Yeast (Chichester, England) · 2015Article
- Role of the yeast DNA repair protein Nej1 in end processing during the repair of DNA double strand breaks by non-homologous end joining.DNA repair · 2015Article
- Double-strand break repair-adox: Restoration of suppressed double-strand break repair during mitosis induces genomic instability.Cancer science · 2014Review
- Genome-wide screens for sensitivity to ionizing radiation identify the fission yeast nonhomologous end joining factor Xrc4.G3 (Bethesda, Md.) · 2014Article
- The C-terminus of Nej1 is critical for nuclear localization and non-homologous end-joining.DNA repair · 2014Article
2 more citing papers are in PubMed but not listed here.
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3 authors.
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Abstract
Saccharomyces cerevisiae DNA ligase IV (LIG4) has been shown previously to be involved in non-homologous DNA end joining and meiosis. The homologous mammalian DNA ligase IV interacts with XRCC4, a protein implicated in V(D)J recombination and double-strand break repair. Here, we report the discovery of LIF1, a S.cerevisiae protein that strongly interacts with the C-terminal BRCT domain of yeast LIG4. LIG4 and LIF1 apparently occur as a heterodimer in vivo. LIF1 shares limited sequence homology with mammalian XRCC4. Disruption of the LIF1 gene abolishes the capacity of cells to recircularize transformed linearized plasmids correctly by non-homologous DNA end joining. Loss of LIF1 is also associated with conditional hypersensitivity of cells to ionizing irradiation and with reduced sporulation efficiency. Thus, with respect to their phenotype, lif1 strains are similar to the previously described lig4 mutants. One function of LIF1 is the stabilization of the LIG4 enzyme. The finding of a XRCC4 homologue in S.cerevisiae now allows for mutational analyses of structure-function relationships in XRCC4-like proteins to define their role in DNA double-strand break repair.
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