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. 2002 Jan;184(2):592-5.
doi: 10.1128/jb.184.2.592-595.2002.

Role of the RecBCD Recombination Pathway in Salmonella Virulence

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Free PMC article

Role of the RecBCD Recombination Pathway in Salmonella Virulence

David A Cano et al. J Bacteriol. .
Free PMC article

Abstract

Mutants of Salmonella enterica lacking the RecBC function are avirulent in mice and unable to grow inside macrophages (N. A. Buchmeier, C. J. Lipps, M. Y. H. So, and F. Heffron, Mol. Microbiol. 7:933-936, 1993). The virulence-related defects of RecBC(-) mutants are not suppressed by sbcB and sbcCD mutations, indicating that activation of the RecF recombination pathway cannot replace the virulence-related function(s) of RecBCD. Functions of the RecF pathway such as RecJ and RecF are not required for virulence. Since the RecBCD pathway, but not the RecF pathway, is known to participate in the repair of double-strand breaks produced during DNA replication, we propose that systemic infection by S. enterica may require RecBCD-mediated recombinational repair to prime DNA replication inside phagocytes. Mutants lacking both RecD and RecJ are also attenuated in mice and are unable to proliferate in macrophages, suggesting that exonucleases V and IX provide alternative functions for RecBCD-mediated recombinational repair during Salmonella infection.

Figures

FIG. 1.
FIG. 1.
Ability of recombination mutants of S. enterica to proliferate in J774.A1 macrophages. Growth, infection, and lysis of J774.A1 mouse macrophages were carried out as described elsewhere (9, 10). The bacterial strains used for infection were SV1445, SV1488, SV4189, SV4190, SV4212, SV4213, SV4192, SV4363, and SV4364. The intracellular proliferation rate (Ipro) was calculated as the ratio of the number of viable intracellular bacteria present at 24 h to the number present at 2 h postinfection. Data are means ± standard deviations of results from two representative experiments. The assay was repeated three times for each strain. wt, wild type.

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