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Mutation Spectrum Induced by Singlet Oxygen in Escherichia coli Deficient in Exonuclease III
Author(s) -
AgnezLima Lucymara F.,
Mascio Paolo Di,
Napolitano Rita L.,
Fuchs Robert P.,
Menck Carlos F. M.
Publication year - 1999
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1111/j.1751-1097.1999.tb08245.x
Subject(s) - exonuclease , ap site , escherichia coli , biology , base excision repair , mutation , pyrimidine dimer , endonuclease , microbiology and biotechnology , plasmid , exonuclease iii , dna , dna repair , genetics , gene , dna polymerase
The repair of singlet oxygen ( 1 O 2 )‐induced DNA lesions requires several enzymes of the nucleotide and base excision repair pathways, including exonuclease III and endonucle‐ase IV that are known apurinic/apyrunidinic‐endonucleases in Escherichia coli. In order to better understand the relevance of exonuclease III on the repair of these lesions, we investigated the mutagenic events that result from the replication of a 1 O 2 ‐damaged plasmid in an exonuclease‐deflcient host ( xth ). The mutation spectrum in the tRNA supF gene target indicated that the absence of exonuclease III does not change the types of mutations induced by 1 O 2 (mostly of G:C ← T:A and G:C ← C:G transver‐sions). However, the spectrum shows that the mutations are scattered in the supF gene, which is significatively different from the one obtained in wild‐type bacteria. Thus, exonuclease III may act on the repair of 1 O 2 ‐induced lesions altering the DNA repair sequence specificity.