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Mutagenesis 2004 19(5):349-354; doi:10.1093/mutage/geh039
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Mutagenesis vol. 19 no. 5 © UK Environmental Mutagen Society 2004; all rights reserved.

Divergent adaptation of Escherichia coli to cyclic ultraviolet light exposures

David Alcántara-Díaz1, Matilde Breña-Valle and Jorge Serment-Guerrero

Departamento de Biología, Instituto Nacional de Investigaciones Nucleares, PO Box 18-1027, CP 11801, México DF, México

The genetic changes taking place during adaptive evolution are particularly interesting in evolutionary biology. As a consequence of adaptive evolution, natural populations of an organism under selective conditions change genetically and phenotypically after a number of generations in order to survive in that particular environment. When a DNA-damaging and mutagenic agent like UV light is experimentally used as a selective factor, natural resistance of bacteria to this agent is normally increased through processes of mutation and selection. Since UV-induced mutagenesis is not restricted to particular chromosomal regions, different UV resistance mechanisms will equally probably evolve as a consequence of cyclic UV irradiation. However, it is also possible that as a consequence of the selective process, one UV resistance mechanism is preferentially selected, causing adaptive convergence of different bacterial cultures. This may occur if the most abundant or lethal kind of DNA lesion is preferentially managed by a particular DNA repair pathway and even by a specific repair enzyme or if resistance mechanisms that decrease bacterial fitness tend to be eliminated from the populations. To examine which of these two alternatives actually takes place, five cultures of Escherichia coli were treated in parallel for 80 successive UV irradiation cycles. At the end, these five cultures gave rise to different grades of UV resistance and after a preliminary characterization we found that adaptation to cyclic UV irradiation was a consequence of selection of advantageous mutations arising in different genes related to repair and replication of DNA.

1 To whom correspondence should be addressed. Tel: +52 5 329 72 30; Fax: +52 5 521 9893; Email: dad{at}nuclear.inin.mx


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