Genetic evidence for the nature, and excision repair, of DNA lesions resulting from incorporation of 5-bromouracil |
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Authors: | Malgorzata Krych Irena Pietrzykowska Jolanta Szyszko and David Shugar |
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Institution: | (1) Institute of Biochemistry and Biophysics, Academy of Sciences, 36 Rakowiecka St., 05-532 Warszawa, Poland |
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Abstract: | Summary
Escherichia coli mutants defective in DNA uracil N-glycosidase (ung
–) or endonuclease VI active against apurinic/apyrimidinic sites in DNA (xthA–) exhibit enhanced sensitivity towards 5-bromodeoxyuridine relative to the wild type strain, pointing to involvement of these enzymes in repair of bromouracil-induced lesions in DNA.Mutants defective in DNA polymerase I, either in polymerizing activity (polAl–) or (5![prime](/content/p49ru832336tt761/xxlarge8242.gif) 3 )-exonuclease activity (polA107–) exhibit unusually high sensitivity (including marked lethality) in the presence of 5-bromodeoxyuridine. The results indicate that DNA polymerase I, and its associated (5 –3 )-exonuclease activity, are involved in repair of bromouracil-induced lesions and are not readily replaced, if at all, by DNA polymerases II and III.Thermosensitive mutant in DNA ligase gene (lig ts7) shows high sensitivity towards 5-bromodeoxyuridine at 42°C indicating the role of the enzyme in repair of bromouracil-induced lesions in DNA.Involvement of DNA uracil N-glycosidase, and endonuclease active against apurinic/apyrimidinic sites in recognition and repair of 5-bromouracil-induced damage permits of some inferences regarding the nature of this damage (lesions), in particular dehalogenation of incorporated bromouracil to uracil residues. |
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