ArticleGenome research2014
Polymerase theta-mediated end joining of replication-associated DNA breaks in C. elegans.
Article in Genome research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 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.
The trial behind it
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
111 citing papers in PubMed, 166 citations in OpenAlex.
- Sam68 stimulates polymerase theta-mediated end-joining by suppressing poison exon inclusion in Polq mRNA.Nucleic acids research · 2026Article
- Microhomology-mediated end joining acts directly on replication forks to repair single-ended double-strand breaks.Molecular cell · 2026Article
- TONSL suppresses polymerase theta-dependent tandem duplications through chromatin-guided repair.Nature communications · 2026Article
- Review
- Division of labor within polymerase theta in repair of CRISPR-induced DNA breaks inPNAS nexus · 2025Article
- FAN1-mediated translesion synthesis and POLQ/HELQ-mediated end joining generate interstrand crosslink-induced mutations.Nature communications · 2025Article
- Structural basis of error-prone DNA synthesis by DNA polymerase θ.Nature communications · 2025Article
- Dynamic interplay of cNHEJ and MMEJ pathways of DNA double-strand break repair during embryonic development in zebrafish.Scientific reports · 2025Article
- GDBr: genomic signature interpretation tool for DNA double-strand break repair mechanisms.Nucleic acids research · 2025Article
- The Evolutionary Potential of Chromoanagenesis.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Replication stress induces POLQ-mediated structural variant formation throughout common fragile sites after entry into mitosis.Nature communications · 2024Article
- Microhomology-Mediated End-Joining Chronicles: Tracing the Evolutionary Footprints of Genome Protection.Annual review of cell and developmental biology · 2024Review
- Polymerase theta is a synthetic lethal target for killing Epstein-Barr virus lymphomas.Journal of virology · 2024Article
- Dynamic stem-loop extension by Pol θ and templated insertion during DNA repair.The Journal of biological chemistry · 2024Article
- Reference-free structural variant detection in microbiomes via long-read co-assembly graphs.Bioinformatics (Oxford, England) · 2024Article
- Discovery of a small-molecule inhibitor that traps Polθ on DNA and synergizes with PARP inhibitors.Nature communications · 2024Article
- Genetic dissection of mutagenic repair and T-DNA capture at CRISPR-induced DNA breaks inPNAS nexus · 2024Article
- Reference-free Structural Variant Detection in Microbiomes via Long-read Coassembly Graphs.bioRxiv : the preprint server for biology · 2024Article
- Genomic consequences associated with Agrobacterium-mediated transformation of plants.The Plant journal : for cell and molecular biology · 2024Review
- POLQ to the rescue for double-strand break repair during mitosis.Nature structural & molecular biology · 2023Article
51 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
DNA lesions that block replication fork progression are drivers of cancer-associated genome alterations, but the error-prone DNA repair mechanisms acting on collapsed replication are incompletely understood, and their contribution to genome evolution largely unexplored. Here, through whole-genome sequencing of animal populations that were clonally propagated for more than 50 generations, we identify a distinct class of deletions that spontaneously accumulate in C. elegans strains lacking translesion synthesis (TLS) polymerases. Emerging DNA double-strand breaks are repaired via an error-prone mechanism in which the outermost nucleotide of one end serves to prime DNA synthesis on the other end. This pathway critically depends on the A-family polymerase theta, which protects the genome against gross chromosomal rearrangements. By comparing the genomes of isolates of C. elegans from different geographical regions, we found that in fact most spontaneously evolving structural variations match the signature of polymerase theta-mediated end joining (TMEJ), illustrating that this pathway is an important source of genetic diversification.
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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.