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Multiple Pathways of Recombination Define Cellular Responses to Cisplatin by Zoran Z Zdraveski; Jill A Mello; Martin G Marinus; John M Essigmann is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.

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Background: Cisplatin is a DNA-damaging drug used for treatment of testicular tumors. The toxicity of cisplatin probably results from its ability to form DNA adducts that inhibit polymerases. Blocked replication represents a particular challenge for tumor cells, which are committed to unremitting division. Recombination provides a mechanism by which replication can proceed despite the presence of lesions and therefore could be significant for managing cisplatin toxicity. Results: Recombination-deficient Escherichia coli mutants were strikingly sensitive to cisplatin when compared with the parental strain. Our data identified both daughter-strand gap and double-strand break recombination pathways as critical for survival following treatment with cisplatin. Although it is established that nucleotide excision repair (NER) significantly protects against cisplatin toxicity, most recombination-deficient strains were as sensitive to the drug as the NER-deficient uvrA mutant. Recombination/NER deficient double mutants were more sensitive to cisplatin than the corresponding single mutants, suggesting that recombination and NER pathways play independent roles in countering cisplatin toxicity

Who reads Multiple Pathways of Recombination Define Cellular Responses to Cisplatin?

Author

Zoran Z Zdraveski; Jill A Mello; Martin G Marinus; John M Essigmann

Publisher

Elsevier Science; Elsevier ; Cell Press; Elsevier BV (ISSN 1074-5521)

Published

2000

Language

EN

Field

Biochemistry, Genetics and Molecular Biology (Life Sciences)