ArticleNucleic acids research2008
Alkylation damage causes MMR-dependent chromosomal instability in vertebrate embryos.
Article in Nucleic acids research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 20 citations in OpenAlex.
- Oxidative Stress, Genetic Factors and Behavioral Responses to Chemical Exposure: Insights into Cancer Development in Zebrafish (Danio Rerio).Biochemical genetics · 2026Review
- Mutation and selection processes regulating short tandem repeats give rise to genetic and phenotypic diversity across species.Journal of evolutionary biology · 2023Review
- In vitro study of human mutL homolog 1 hypermethylation in inducing drug resistance of esophageal carcinoma.Irish journal of medical science · 2017Article
- A novel DNA damage response mediated by DNA mismatch repair in Caenorhabditis elegans: induction of programmed autophagic cell death in non-dividing cells.Genes & cancer · 2015Article
- N-nitroso-N-ethylurea activates DNA damage surveillance pathways and induces transformation in mammalian cells.BMC cancer · 2014Article
- Distinct pathways for repairing mutagenic lesions induced by methylating and ethylating agents.Mutagenesis · 2013Article
- Aberrant methylation of different DNA repair genes demonstrates distinct prognostic value for esophageal cancer.Digestive diseases and sciences · 2011Article
- Use of RecA fusion proteins to induce genomic modifications in zebrafish.Nucleic acids research · 2011Article
- Reverse genetics in zebrafish by TILLING.Briefings in functional genomics & proteomics · 2008Review
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
S(N)1-type alkylating agents, like N-methyl-N-nitrosourea (MNU) and N-ethyl-N-nitrosourea (ENU), are potent mutagens. Exposure to alkylating agents gives rise to O(6)-alkylguanine, a modified base that is recognized by DNA mismatch repair (MMR) proteins but is not repairable, resulting in replication fork stalling and cell death. We used a somatic mutation detection assay to study the in vivo effects of alkylation damage on lethality and mutation frequency in developing zebrafish embryos. Consistent with the damage-sensing role of the MMR system, mutant embryos lacking the MMR enzyme MSH6 displayed lower lethality than wild-type embryos after exposure to ENU and MNU. In line with this, alkylation-induced somatic mutation frequencies were found to be higher in wild-type embryos than in the msh6 loss-of-function mutants. These mutations were found to be chromosomal aberrations that may be caused by chromosomal breaks that arise from stalled replication forks. As these chromosomal breaks arise at replication, they are not expected to be repaired by non-homologous end joining. Indeed, Ku70 loss-of-function mutants were found to be equally sensitive to ENU as wild-type embryos. Taken together, our results suggest that in vivo alkylation damage results in chromosomal instability and cell death due to aberrantly processed MMR-induced stalled replication forks.
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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.