Mutation Spectrum Induced by Singlet Oxygen in Escherichia coli Deficient in Exonuclease III

Authors

  • Lucymara F. Agnez-Lima,

    1. Departamento de Microbiologia, Institute de Ciencias Biomedicas, Universidade de Sao Paulo, Sao Paulo, Brazil
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    • †Departamento de Biologia Celular e GenCtica, Centro de Biocisncias, Universidade Federal do Rio Grande do Norte, Natal, RN, Brazil.

  • Paolo Di Mascio,

    1. Departamento de Bioquimica, Institute de Qufmica, Universidade de Sao Paulo, Sao Paulo, Brazil
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  • Rita L. Napolitano,

    1. Ecole Superieure de Biotechnologie de Strasbourg, Strasbourg, France
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  • Robert P. Fuchs,

    1. Ecole Superieure de Biotechnologie de Strasbourg, Strasbourg, France
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  • Carlos F. M. Menck

    1. Departamento de Microbiologia, Institute de Ciencias Biomedicas, Universidade de Sao Paulo, Sao Paulo, Brazil
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    • *To whom correspondence should be addressed at: Departamento de Microbiologia, ICB2, USP, Av. Prof. Lineu Prestes, 1374, Sao Paulo, 05508-900, SP, Brazil. Fax; 55.11.818.7354; e-mail:cfmmenck@usp.br


Abstract

The repair of singlet oxygen (1O2)-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 1O2-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 1O2 (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 1O2-induced lesions altering the DNA repair sequence specificity.

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