ArticleCell reports2016
Polq-Mediated End Joining Is Essential for Surviving DNA Double-Strand Breaks during Early Zebrafish Development.
Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 38 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
38 citing papers in PubMed.
- DNA polymerase theta (Polθ): a novel candidate for targeted cancer therapy.Cancer biology & therapy · 2026Review
- Interfering with DNA repair pathways to enhance CRISPR-Cas9-mediated homology-directed repair in a chelicerate genetic model.iScience · 2026Article
- Precise, predictable genome integrations by deep-learning-assisted design of microhomology-based templates.Nature biotechnology · 2026Article
- Genetically encoded affinity reagents are a toolkit for visualizing and manipulating endogenous protein function in vivo.Nature communications · 2025Article
- Identifying optimal conditions for precise knock-in of exogenous DNA into the zebrafish genome.Development (Cambridge, England) · 2025Article
- Article
- Dynamic interplay of cNHEJ and MMEJ pathways of DNA double-strand break repair during embryonic development in zebrafish.Scientific reports · 2025Article
- Zebrafish Polymerase Theta and human Polymerase Theta: Orthologues with homologous function.PloS one · 2025Article
- Barcoding Notch signaling in the developing brain.Development (Cambridge, England) · 2024Article
- Microhomology-Mediated End-Joining Chronicles: Tracing the Evolutionary Footprints of Genome Protection.Annual review of cell and developmental biology · 2024Review
- Dynamic stem-loop extension by Pol θ and templated insertion during DNA repair.The Journal of biological chemistry · 2024Article
- The cGAS-Ku80 complex regulates the balance between two end joining subpathways.Cell death and differentiation · 2024Article
- Templated insertions-DNA repair gets acrobatic.Environmental and molecular mutagenesis · 2024Review
- Developmental progression of DNA double-strand break repair deciphered by a single-allele resolution mutation classifier.Nature communications · 2024Article
- Transformation and regeneration of DNA polymerase Θ mutant rice plants.Plant direct · 2023Article
- Structural basis of DNA polymerase θ mediated DNA end joining.Nucleic acids research · 2023Article
- Genome Protection by DNA Polymerase θ.Annual review of genetics · 2022Review
- CRISPR-Cas12a induced DNA double-strand breaks are repaired by multiple pathways with different mutation profiles in Magnaporthe oryzae.Nature communications · 2022Article
- Contribution of Microhomology to Genome Instability: Connection between DNA Repair and Replication Stress.International journal of molecular sciences · 2022Review
- DNA Polymerase Theta Plays a Critical Role in Pancreatic Cancer Development and Metastasis.Cancers · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
2 authors.
Funding
Abstract
Error-prone repair of DNA double-strand breaks (DSBs) has been postulated to occur through classical non-homologous end joining (NHEJ) in systems ranging from nematode somatic tissues to zebrafish embryos. Contrary to this model, we show that zebrafish embryos mutant for DNA polymerase theta (Polq), a critical component of alternative end joining (alt-EJ), cannot repair DSBs induced by CRISPR/Cas9 or ionizing radiation. In the absence of DSBs, polq mutants are phenotypically normal, but they do not survive mutagenesis and display dramatic differences in the mutation profiles compared with the wild-type. These results show that alt-EJ repair is essential and dominant during the early development of a vertebrate.
Identifiers
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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.