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Research Article

Survival and SOS response induction in ultraviolet B irradiated Escherichia coli cells with defective repair mechanisms

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Pages 321-328 | Received 22 Feb 2015, Accepted 26 Jan 2016, Published online: 11 Mar 2016
 

Abstract

Purpose In this paper, the contribution of different genes involved in DNA repair for both survival and SOS induction in Escherichia coli mutants exposed to ultraviolet B radiation (UVB, [wavelength range 280–315 nm]) was evaluated.

Materials and methods E. coli strains defective in uvrA, oxyR, recO, recN, recJ, exoX, recB, recD or xonA genes were used to determine cell survival. All strains also had the genetic sulA::lacZ fusion, which allowed for the quantification of SOS induction through the SOS Chromotest.

Results Five gene products were particularly important for survival, as follows: UvrA > RecB > RecO > RecJ > XonA. Strains defective in uvrA and recJ genes showed elevated SOS induction compared with the wild type, which remained stable for up to 240 min after UVB-irradiation. In addition, E. coli strains carrying the recO or recN mutation showed no SOS induction.

Conclusions The nucleotide excision and DNA recombination pathways were equally used to repair UVB-induced DNA damage in E. coli cells. The sulA gene was not turned off in strains defective in UvrA and RecJ. RecO protein was essential for processing DNA damage prior to SOS induction. In this study, the roles of DNA repair proteins and their contributions to the mechanisms that induce SOS genes in E. coli are proposed.

Acknowledgements

This work was supported by the “Vicerrectoría de Investigaciones y Extensión de la Universidad Industrial de Santander” and by the “Patrimonio Autónomo Fondo Nacional de Financiamiento para la Ciencia, la Tecnología y la Innovación, Francisco José de Caldas” (Contract No. RC-0572–2012). The Ministerio de Ambiente y Desarrollo Sostenible (MADS) of Colombia permitted the access to genetic resources and derived products during this scientific research (Contract No. 101, Resolution No. 0812).

Disclosure statement

The authors report no conflict of interest. The authors alone are responsible for the content and writing of the paper.

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