ArticleProceedings of the National Academy of Sciences of the United States of America2012
Y265C DNA polymerase beta knockin mice survive past birth and accumulate base excision repair intermediate substrates.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 30 citations in OpenAlex.
- DNA polymerase β suppresses somatic indels at CpG dinucleotides in developing cortical neurons.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Unfilled gaps by polβ lead to aberrant ligation by LIG1 at the downstream steps of base excision repair pathway.Nucleic acids research · 2024Article
- Mouse models to explore the biological and organismic role of DNA polymerase beta.Environmental and molecular mutagenesis · 2024Review
- Polβ/XRCC1 heterodimerization dictates DNA damage recognition and basal Polβ protein levels without interfering with mouse viability or fertility.DNA repair · 2023Article
- The hematopoietic compartment is sufficient for lupus development resulting from the POLB-Y265C mutation.PloS one · 2022Article
- DNA glycosylase deficiency leads to decreased severity of lupus in the Polb-Y265C mouse model.DNA repair · 2021Article
- Symmetric activity of DNA polymerases at and recruitment of exonuclease ExoR and of PolA to the Bacillus subtilis replication forks.Nucleic acids research · 2019Article
- Mitochondria in the signaling pathways that control longevity and health span.Ageing research reviews · 2019Review
- POLE proofreading defects: Contributions to mutagenesis and cancer.DNA repair · 2019Review
- DNA polymerase beta participates in DNA End-joining.Nucleic acids research · 2018Article
- Genome Stability by DNA Polymerase β in Neural Progenitors Contributes to Neuronal Differentiation in Cortical Development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- DNA repair and systemic lupus erythematosus.DNA repair · 2017Review
- Base excision repair of oxidative DNA damage: from mechanism to disease.Frontiers in bioscience (Landmark edition) · 2017Review
- Mutation of DNA Polymerase β R137Q Results in Retarded Embryo Development Due to Impaired DNA Base Excision Repair in Mice.Scientific reports · 2016Article
- Heterozygosity for a hypomorphic Polβ mutation reduces the expansion frequency in a mouse model of the Fragile X-related disorders.PLoS genetics · 2015Article
- A new conceptual framework for investigating complex genetic disease.Frontiers in genetics · 2015Article
- Mutation of POLB causes lupus in mice.Cell reports · 2014Article
- Cellular roles of DNA polymerase beta.The Yale journal of biology and medicine · 2013Review
- Base excision repair in the mammalian brain: implication for age related neurodegeneration.Mechanisms of ageing and development · 2013Article
- Epistatic role of base excision repair and mismatch repair pathways in mediating cisplatin cytotoxicity.Nucleic acids research · 2013Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
DNA is susceptible to damage by a wide variety of chemical agents that are generated either as byproducts of cellular metabolism or exposure to man-made and harmful environments. Therefore, to maintain genomic integrity, having reliable DNA repair systems is important. DNA polymerase β is known to be a key player in the base excision repair pathway, and mice devoid of DNA polymerase beta do not live beyond a few hours after birth. In this study, we characterized mice harboring an impaired pol β variant. This Y265C pol β variant exhibits slow DNA polymerase activity but WT lyase activity and has been shown to be a mutator polymerase. Mice expressing Y265C pol β are born at normal Mendelian ratios. However, they are small, and 60% die within a few hours after birth. Slow proliferation and significantly increased levels of cell death are observed in many organs of the E14 homozygous embryos compared with WT littermates. Mouse embryo fibroblasts prepared from the Y265C pol β embryos proliferate at a rate slower than WT cells and exhibit a gap-filling deficiency during base excision repair. As a result of this, chromosomal aberrations and single- and double-strand breaks are present at significantly higher levels in the homozygous mutant versus WT mouse embryo fibroblasts. This is study in mice is unique in that two enzymatic activities of pol β have been separated; the data clearly demonstrate that the DNA polymerase activity of pol β is essential for survival and genome stability.
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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.