ArticleOncogene2001
Elevated mutant frequencies and increased C : G-->T : A transitions in Mlh1-/- versus Pms2-/- murine small intestinal epithelial cells.
Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 36 citations in OpenAlex.
- Efficient prime editing in two-cell mouse embryos using PEmbryo.Nature biotechnology · 2024Article
- Mismatch repair-signature mutations activate gene enhancers across human colorectal cancer epigenomes.eLife · 2019Article
- Mutational signatures of DNA mismatch repair deficiency inGenome research · 2018Article
- Deficiency of the DNA repair protein nibrin increases the basal but not the radiation induced mutation frequency in vivo.Mutation research · 2014Article
- The lower bound to the evolution of mutation rates.Genome biology and evolution · 2011Article
- DNA replication fidelity and cancer.Seminars in cancer biology · 2010Review
- TagRecon: high-throughput mutation identification through sequence tagging.Journal of proteome research · 2010Article
- Article
- Differing patterns of genetic instability in mice deficient in the mismatch repair genes Pms2, Mlh1, Msh2, Msh3 and Msh6.Carcinogenesis · 2006Article
- Accelerated growth of intestinal tumours after radiation exposure in Mlh1-knockout mice: evaluation of the late effect of radiation on a mouse model of HNPCC.International journal of experimental pathology · 2006Article
- Chloroplast DNA base substitutions: an experimental assessment.Molecular genetics and genomics : MGG · 2005Article
- Article
- Mbd4 inactivation increases Cright-arrowT transition mutations and promotes gastrointestinal tumor formation.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Elevated mutant frequencies and predominance of G:C to A:T transition mutations in Msh6(-/-) small intestinal epithelium.Oncogene · 2002Article
- Loss of heterozygosity and point mutation at Aprt locus in T cells and fibroblasts of Pms2-/- mice.Oncogene · 2002Article
- Embryonic stem cells and somatic cells differ in mutation frequency and type.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Multiple mutations are common at mouse Aprt in genotoxin-exposed mismatch repair deficient cells.Oncogene · 2002Article
- Mutational fingerprints of aging.Nucleic acids research · 2002Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Mutations in DNA mismatch repair (MMR) genes are associated with increased genomic instability and susceptibility to cancer. Mice rendered deficient in either Mlh1 or Pms2 as a result of gene targeting are prone to tumorigenesis, particularly, lymphomas. In addition, although Mlh1-/- mice also develop small intestinal adenomas and adenocarcinomas, Pms2-/- animals remain free of such tumors. To establish whether this phenotypic dichotomy might be associated with a quantitative and/or qualitative difference in genomic instability in these mice, we determined small intestinal epithelial cell DNA mutant frequency and mutation spectrum using a transgenic lambda-phage lacI reporter system. Mutant frequencies obtained from both Mlh1-/- and Pms2-/- mice revealed elevations of 18- and 13-fold, respectively, as compared to their wild-type littermates. Interestingly, we found that C : G-->T : A transitions were significantly elevated in Mlh1-/- mice, accounting in large measure for the 1.5-fold lacI mutant frequency increase seen in these animals. We hypothesize that the increased level of C : G-->T : A mutations may explain, in part, why Mlh1-/- mice, but not Pms2-/- mice, develop small intestinal tumors. Furthermore, the difference in the lacI mutational spectrum of Mlh1-/- and Pms2-/- mice suggests that other MutL-like heterodimers may play important roles in the repair of G : T mispairs arising within murine small intestinal epithelial cells.
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