ArticleNucleic acids research2017
Systematic analysis of DNA crosslink repair pathways during development and aging in Caenorhabditis elegans.
Article in Nucleic acids research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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
19 citing papers in PubMed, 27 citations in OpenAlex.
- FAN1-mediated translesion synthesis and POLQ/HELQ-mediated end joining generate interstrand crosslink-induced mutations.Nature communications · 2025Article
- Loss of DNA glycosylases improves health and cognitive function in a C. elegans model of human tauopathy.Nucleic acids research · 2024Article
- The critical role of the iron-sulfur cluster and CTC components in DOG-1/BRIP1 function in Caenorhabditis elegans.Nucleic acids research · 2024Article
- The DREAM complex functions as conserved master regulator of somatic DNA-repair capacities.Nature structural & molecular biology · 2023Article
- Lineage Landscape: a comprehensive database that records lineage commitment across species.Nucleic acids research · 2023Article
- Differential requirement for BRCA1-BARD1 E3 ubiquitin ligase activity in DNA damage repair and meiosis in the Caenorhabditis elegans germ line.PLoS genetics · 2023Article
- Loss of NSE-4 Perturbs Genome Stability and DNA Repair inInternational journal of molecular sciences · 2022Article
- DNA repair, recombination, and damage signaling.Genetics · 2022Review
- Analysis of representative mutants for key DNA repair pathways on healthspan in Caenorhabditis elegans.Mechanisms of ageing and development · 2021Article
- The base excision repair process: comparison between higher and lower eukaryotes.Cellular and molecular life sciences : CMLS · 2021Review
- Histone demethylase AMX-1 is necessary for proper sensitivity to interstrand crosslink DNA damage.PLoS genetics · 2021Article
- Efficient collection of a large number of mutations by mutagenesis of DNA damage response defective animals.Scientific reports · 2021Article
- Why Concurrent CDDP and Radiotherapy Has Synergistic Antitumor Effects: A Review of In Vitro Experimental and Clinical-Based Studies.International journal of molecular sciences · 2021Review
- Nucleotide Excision Repair, XPA-1, and the Translesion Synthesis Complex, POLZ-1 and REV-1, Are Critical for Interstrand Cross-Link Repair inBiochemistry · 2020Article
- Unhooking of an interstrand cross-link at DNA fork structures by the DNA glycosylase NEIL3.DNA repair · 2020Article
- The Base Excision Repair Pathway in the NematodeFrontiers in cell and developmental biology · 2020Review
- Nucleotide excision repair genes shaping embryonic development.Open biology · 2019Review
- Restoration of Proteostasis in the Endoplasmic Reticulum Reverses an Inflammation-Like Response to Cytoplasmic DNA inGenetics · 2019Article
- MPK-1/ERK pathway regulates DNA damage response during development through DAF-16/FOXO.Nucleic acids research · 2018Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
DNA interstrand crosslinks (ICLs) are generated by endogenous sources and chemotherapeutics, and pose a threat to genome stability and cell survival. Using Caenorhabditis elegans mutants, we identify DNA repair factors that protect against the genotoxicity of ICLs generated by trioxsalen/ultraviolet A (TMP/UVA) during development and aging. Mutations in nucleotide excision repair (NER) components (e.g. XPA-1 and XPF-1) imparted extreme sensitivity to TMP/UVA relative to wild-type animals, manifested as developmental arrest, defects in adult tissue morphology and functionality, and shortened lifespan. Compensatory roles for global-genome (XPC-1) and transcription-coupled (CSB-1) NER in ICL sensing were exposed. The analysis also revealed contributions of homologous recombination (BRC-1/BRCA1), the MUS-81, EXO-1, SLX-1 and FAN-1 nucleases, and the DOG-1 (FANCJ) helicase in ICL resolution, influenced by the replicative-status of the cell/tissue. No obvious or critical role in ICL repair was seen for non-homologous end-joining (cku-80) or base excision repair (nth-1, exo-3), the Fanconi-related proteins BRC-2 (BRCA2/FANCD1) and FCD-2 (FANCD2), the WRN-1 or HIM-6 (BLM) helicases, or the GEN-1 or MRT-1 (SNM1) nucleases. Our efforts uncover replication-dependent and -independent ICL repair networks, and establish nematodes as a model for investigating the repair and consequences of DNA crosslinks in metazoan development and in adult post-mitotic and proliferative germ cells.
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Registered trials
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