Suppression of human DNA alkylation-repair defects by Escherichia coli DNA-repair genes.
- 1 August 1986
- journal article
- research article
- Published by Proceedings of the National Academy of Sciences in Proceedings of the National Academy of Sciences
- Vol. 83 (15) , 5607-5610
- https://doi.org/10.1073/pnas.83.15.5607
Abstract
The ada-alkB operon protects Escherichia coli against the effects of many alkylating agents. We have subcloned it into the pSV2 mammalian expression vector to yield pSV2ada-alkB, and this plasmid has been introduced into Mer- HeLa S3 cells, which are extremely sensitive to killing and induction of sister chromatid exchange by alkylating agents. One transformant (the S3-9 cell line) has several integrated copies of pSV2ada-alkB and was found to express a very high level of the ada gene product, the 39-kDa O6-methylguanine-DNA methyltransferase. S3-9 cells were found to have become resistant to killing and induction of sister chromatid exchange by two alkylating agents, N-methyl-N''-nitro-N-nitrosoguanidine and N,N''-bis(2-chloroethyl)-N-nitrosourea. This shows that bacterial DNA alkylation-repair genes are able to suppress the alkylation-repair defects in human Mer- cells.This publication has 31 references indexed in Scilit:
- Expression of the E. coli O6-methylguanine-methylphosphotriester methyltransferase gene in mammalian cellsCarcinogenesis: Integrative Cancer Research, 1986
- DNA-mediated transfer and expression of a human DNA repair gene that demethylates O6-methylguanine.Molecular and Cellular Biology, 1985
- Genetic complementation of UV-induced DNA repair in Chinese hamster ovary cells by the denV gene of phage T4.Proceedings of the National Academy of Sciences, 1985
- Possible depletion of a DNA repair enzyme in human lymphoma cells by subversive repair.Proceedings of the National Academy of Sciences, 1985
- Cloning of theE. coliO6-methylguanine and methylphosphotriester methyltransferase gene using a functional DNA repair assayNucleic Acids Research, 1985
- The cytotoxic and mutagenic effects of alkylating agents on human lymphoid cells are caused by different DNA lesionsCarcinogenesis: Integrative Cancer Research, 1985
- Depletion of O6-methylguanine-DNA-methyltransferase in human fibroblasts increases the mutagenic response to N-methyl-N'-nitro-N-nitrosoguanidineCarcinogenesis: Integrative Cancer Research, 1985
- Methyl phosphotriesters in alkylated DNA are repaired by the Ada regulatory protein ofE. coliNucleic Acids Research, 1985
- In vivo mutagenesis by O6-methylguanine built into a unique site in a viral genome.Proceedings of the National Academy of Sciences, 1984
- Adaptive response to alkylating agents involves alteration in situ of O6-methylguanine residues in DNANature, 1979