ArticleJournal of bacteriology1998
The Pol beta-14 dominant negative rat DNA polymerase beta mutator mutant commits errors during the gap-filling step of base excision repair in Saccharomyces cerevisiae.
Article in Journal of bacteriology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 15 citations in OpenAlex.
- Heterozygosity for a hypomorphic Polβ mutation reduces the expansion frequency in a mouse model of the Fragile X-related disorders.PLoS genetics · 2015Article
- Biological and therapeutic relevance of nonreplicative DNA polymerases to cancer.Antioxidants & redox signaling · 2013Review
- Functional analyses of human DNA repair proteins important for aging and genomic stability using yeast genetics.DNA repair · 2012Review
- Mutagenic specificity of endogenously generated abasic sites in Saccharomyces cerevisiae chromosomal DNA.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Expression of DNA polymerase {beta} cancer-associated variants in mouse cells results in cellular transformation.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- The role of DNA polymerase beta in determining sensitivity to ionizing radiation in human tumor cells.Nucleic acids research · 2002Article
- Enzymatic properties of rat DNA polymerase beta mutants obtained by randomized mutagenesis.Nucleic acids research · 2001Article
- DNA polymerase mu (Pol mu), homologous to TdT, could act as a DNA mutator in eukaryotic cells.The EMBO journal · 2000Article
- The Tyr-265-to-Cys mutator mutant of DNA polymerase beta induces a mutator phenotype in mouse LN12 cells.Proceedings of the National Academy of Sciences of the United States of America · 1999Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
We demonstrated recently that dominant negative mutants of rat DNA polymerase beta (Pol beta) interfere with repair of alkylation damage in Saccharomyces cerevisiae. To identify the alkylation repair pathway that is disrupted by the Pol beta dominant negative mutants, we studied the epistatic relationship of the dominant negative Pol beta mutants to genes known to be involved in repair of DNA alkylation damage in S. cerevisiae. We demonstrate that the rat Pol beta mutants interfere with the base excision repair pathway in S. cerevisiae. In addition, expression of one of the Pol beta dominant negative mutants, Pol beta-14, increases the spontaneous mutation rate of S. cerevisiae whereas expression of another Pol beta dominant negative mutant, Pol beta-TR, does not. Expression of the Pol beta-14 mutant in cells lacking APN1 activity does not result in an increase in the spontaneous mutation rate. These results suggest that gaps are required for mutagenesis to occur in the presence of Pol beta-14 but that it is not merely the presence of a gap that results in mutagenesis. Our results suggest that mutagenesis can occur during the gap-filling step of base excision repair in vivo.
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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.