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Published online ahead of print on 5 November 2009 as doi:10.1099/mic.0.035196-0
Microbiology (2009), DOI 10.1099/mic.0.035196-0
© 2009 Society for General Microbiology

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Microbiology 0 (2009), mic.0.035196; DOI  10.1099/mic.0.035196-0
© 2009 Society for General Microbiology


The SOS response of Listeria monocytogenes is involved in stress resistance and mutagenesis

Stijn van der Veen1,5, Saskia van Schalkwijk2, Douwe Molenaar2, Willem M. de Vos1, Tjakko Abee3 and Marjon HJ Wells-Bennik4

1 Wageningen University & Research Centre;
2 Nizo food research;
3 Wageningen University;
4 NIZO

The SOS response is a conserved pathway that is activated under certain stress conditions and is regulated by the repressor LexA and the activator RecA. The food-borne pathogen Listeria monocytogenes contains RecA and LexA homologs, but their roles in Listeria have not been established. In this study, we identified the SOS regulon in L. monocytogenes by comparing the transcription profiles of the wild-type strain and the {Delta}recA mutant strain after exposure to the DNA damaging agent mitomycin C. In agreement with studies in other bacteria, we identified an imperfect palindrome AATAAGAACATATGTTCGTTT as the SOS operator sequence. The SOS regulon of L. monocytogenes consists of 29 genes in 16 LexA regulated operons, encoding proteins with functions in translesion DNA synthesis and DNA repair. We furthermore identified a role for the product of the LexA regulated gene yneA in cell elongation and inhibition of cell division. As anticipated, RecA of L. monocytogenes plays a role in mutagenesis; {Delta}recA cultures showed considerably lower rifampicin and streptomycin resistant fractions than the wild-type cultures. The SOS response is activated after stress exposure as shown by recA- and yneA-promoter reporter studies. Subsequently, stress survival studies showed {Delta}recA mutant cells to be less resistant to heat, H2O2, and acid exposure than wild-type cells. Our results indicate that the SOS response of L. monocytogenes contributes to survival upon exposure to a range of stresses, thereby likely contributing to its persistence in the environment and in the host.

5 E-mail: stijn.vanderveen{at}wur.nl







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