This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Vandenbosch, J L Articles by Jones, G W Search for Related Content PubMed PubMed Citation Articles by Vandenbosch, J L Articles by Jones, G W

 Previous Article  |  Next Article 

Infect Immun. 1989 March; 57(3): 850-857

Sequence analysis of rsk, a portion of the 95-kilobase plasmid of Salmonella typhimurium associated with resistance to the bactericidal activity of serum.

Department of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor 48109.

ABSTRACT

Increased sensitivity to killing by human serum complement occurs in Salmonella typhimurium strains in which the 95-kilobase virulence plasmid is integrated into the chromosome. This phenotypic change appears to be due to alterations in plasmid gene expression and is reversed by the presence of an autonomous plasmid bearing a cloned region of the virulence plasmid. Accordingly, this region has been termed rsk for reduced serum killing. Sequence analysis of the region reveals that rsk is composed of a series of direct 10-base-pair (bp) repeats with a 21-nucleotide periodicity. Two adjacent repeats are identical, but increasing loss of conservation is apparent with increased distance both 5' and 3' of these highly conserved 10-mers. The smallest isolated sequence which restores the serum-resistant phenotype is only 66 bp long and contains the two identical 10-mers and one degenerate 10-mer (8 of 10 bp conserved) 3' of these. The minimal rsk region of 66 bp does not appear to contain a coding sequence, or a promoter, for a structural gene. It is proposed that the minimal rsk is an isolated regulatory site involved in the regulation of the serum resistance of S. typhimurium. Integration of the 95-kilobase plasmid disrupts the normal regulation of virulence plasmid genes, resulting in an increase in the killing of the bacteria by complement activated by the classical pathway. The introduction of the minimal rsk on a multiple-copy plasmid restores resistance to serum killing, possibly through the titration of a trans-acting regulatory factor.

This article has been cited by other articles:

• Nishio, M., Okada, N., Miki, T., Haneda, T., Danbara, H. (2005). Identification of the outer-membrane protein PagC required for the serum resistance phenotype in Salmonella enterica serovar Choleraesuis. Microbiology 151: 863-873 [Abstract] [Full Text]  
• Chiu, C.-H., Su, L.-H., Chu, C. (2004). Salmonella enterica Serotype Choleraesuis: Epidemiology, Pathogenesis, Clinical Disease, and Treatment. Clin. Microbiol. Rev. 17: 311-322 [Abstract] [Full Text]  
• Chu, C., Hong, S.-F., Tsai, C., Lin, W.-S., Liu, T.-P., Ou, J. T. (1999). Comparative Physical and Genetic Maps of the Virulence Plasmids of Salmonella enterica Serovars Typhimurium, Enteritidis, Choleraesuis, and Dublin. Infect. Immun. 67: 2611-2614 [Abstract] [Full Text]