ArticleNucleic acids research2022
Catalytically inactive DNA ligase IV promotes DNA repair in living cells.
Article in Nucleic acids research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
- Transcriptional regulation of Ligase IV by an intronic regulatory element directs thymocyte development.Genes and immunity · 2025Article
- Article
- The mammalian Ku70 C-terminus SAP domain is required to repair DNA damage.Nucleic acids research · 2025Article
- Joining of DNA breaks- interplay between DNA ligases and poly (ADP-ribose) polymerases.DNA repair · 2025Review
- Lig3-dependent rescue of mouse viability and DNA double-strand break repair by catalytically inactive Lig4.Nucleic acids research · 2025Article
- Multivalent interactions of the disordered regions of XLF and XRCC4 foster robust cellular NHEJ and drive the formation of ligation-boosting condensates in vitro.Nature structural & molecular biology · 2024Article
- DNA-PK: A synopsis beyond synapsis.DNA repair · 2024Review
- Single-molecule imaging reveals the kinetics of non-homologous end-joining in living cells.bioRxiv : the preprint server for biology · 2024Article
- Structural role for DNA Ligase IV in promoting the fidelity of non-homologous end joining.Nature communications · 2024Article
- Mammalian DNA ligases; roles in maintaining genome integrity.Journal of molecular biology · 2024Review
- ALDH1A1 drives prostate cancer metastases and radioresistance by interplay with AR- and RAR-dependent transcription.Theranostics · 2024Article
- Review
- Two distinct long-range synaptic complexes promote different aspects of end processing prior to repair of DNA breaks by non-homologous end joining.Molecular cell · 2023Article
- The DNA binding domain and the C-terminal region of DNA Ligase IV specify its role in V(D)J recombination.PloS one · 2023Article
- The flexible and iterative steps within the NHEJ pathway.Progress in biophysics and molecular biologyArticle
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
Abstract
DNA double strand breaks (DSBs) are induced by external genotoxic agents (ionizing radiation or genotoxins) or by internal processes (recombination intermediates in lymphocytes or by replication errors). The DNA ends induced by these genotoxic processes are often not ligatable, requiring potentially mutagenic end-processing to render ends compatible for ligation by non-homologous end-joining (NHEJ). Using single molecule approaches, Loparo et al. propose that NHEJ fidelity can be maintained by restricting end-processing to a ligation competent short-range NHEJ complex that 'maximizes the fidelity of DNA repair'. These in vitro studies show that although this short-range NHEJ complex requires DNA ligase IV (Lig4), its catalytic activity is dispensable. Here using cellular models, we show that inactive Lig4 robustly promotes DNA repair in living cells. Compared to repair products from wild-type cells, those isolated from cells with inactive Lig4 show a somewhat increased fraction that utilize micro-homology (MH) at the joining site consistent with alternative end-joining (a-EJ). But unlike a-EJ in the absence of NHEJ, a large percentage of joints isolated from cells with inactive Lig4 occur with no MH - thus, clearly distinct from a-EJ. Finally, biochemical assays demonstrate that the inactive Lig4 complex promotes the activity of DNA ligase III (Lig3).
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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.