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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Role of ompR-dependent genes in Salmonella typhimurium virulence: mutants deficient in both ompC and ompF are attenuated in vivo.

A Salmonella typhimurium strain harboring stable mutations in both ompC and ompF was constructed from the mouse-virulent strain S. typhimurium SL1344. When administered orally to BALB/c mice the strain was attenuated, with the 50% lethal dose (LD50) reduced by approximately 1,000-fold. However, the intravenous LD50 was reduced only by approximately 10-fold. The ompC ompF mutant persisted in murine tissues for several weeks following oral challenge, and mice immunized with this mutant were well protected against challenge with virulent SL1344. A strain harboring a stable mutation in tppB behaved in a manner similar to that of strain SL1344 in vivo, while a strain harboring mutations in ompC, ompF, and tppB behaved as an ompC ompF mutant in vivo, indicating that the tppB operon is not required for virulence in S. typhimurium.[1]

References

  1. Role of ompR-dependent genes in Salmonella typhimurium virulence: mutants deficient in both ompC and ompF are attenuated in vivo. Chatfield, S.N., Dorman, C.J., Hayward, C., Dougan, G. Infect. Immun. (1991) [Pubmed]
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