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http://dx.doi.org/10.4014/kjmb.1110.10004

Mutation of the invF Gene Encoding a Salmonella Pathogenicity Island 1 (SPI1) Activator Increases Expression of the SPI2 Gene, sseA  

Han, Ah-Reum (Radiation Research Division for Biotechnology, Korea Atomic Research Institute)
Joe, Min-Ho (Radiation Research Division for Biotechnology, Korea Atomic Research Institute)
Kim, Dong-Ho (Radiation Research Division for Biotechnology, Korea Atomic Research Institute)
Baik, Sang-Ho (Department of Food Science and Human Nutrition, Chonbuk National University)
Lim, Sang-Yong (Radiation Research Division for Biotechnology, Korea Atomic Research Institute)
Publication Information
Microbiology and Biotechnology Letters / v.40, no.1, 2012 , pp. 70-75 More about this Journal
Abstract
In Salmonella enterica, many genes encoded within Salmonella pathogenicity islands (SPI) 1 and 2 are required to cause a range of diseases in a variety of hosts. The SPI1-encoded regulator HilD activates both the SPI1 and 2 genes at different times during growth in Luria-Bertani (LB) media. In this study, the expression levels of hilD during growth in LB were investigated. The data suggest that hilD expression is induced in the early stationary phase and decreases in the late stationary phase, when sseA, an SPI2 gene, is maximally expressed. However, HilD could act as an activator of sseA expression in the late stationary phase despite being present at low levels. SseA expression was investigated in SPI1 regulator mutant strains, hilA, hilD and invF mutants. As expected, hilD mutation decreased sseA expression. However, we found that invF mutation caused a 1.5-fold increase in sseA expression in not only LB but also M9 minimal media, which is thought to resemble an intracellular environment. InvF overexpression restored sseA expression to wild-type levels in an invF mutant but did not cause an additional reduction in sseA expression. These results suggest that SPI1 controls SPI2 expression either positively or negatively.
Keywords
Salmonella Typhimurium; Salmonella pathogenicity island (SPI); invF;
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Times Cited By KSCI : 1  (Citation Analysis)
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1 Beuzon, C. R., G. Banks, J. Deiwick, M. Hensel, and D. W. Holden. 1999. pH-dependent secretion of SseB, a product of the SPI-2 type III secretion system of Salmonella typhimurium. Mol. Microbiol. 33: 806-816.
2 Boddicker, J. D., B. M. Knosp, and B. D. Jones. 2003. Transcription of the Salmonella invasion gene activator, hilA, requires HilD activation in the absence of negative regulators. J. Bacteriol. 185: 525-533.
3 Bustamante, V. H., L. C. Martinez, F. J. Santana, L. A. Knodler, O. Steele-Mortimer, and J. L. Puente. 2008. HilDmediated transcriptional cross-talk between SPI-1 and SPI-2. Proc. Natl. Acad. Sci. USA. 105: 14591-14596.
4 Darwin, K. H. and V. L. Miller.1999. InvF is required for expression of genes encoding proteins secreted by the SPI1 type III secretion apparatus in Salmonella typhimurium. J. Bacteriol. 181: 4949-4954.
5 Datsenko, K. A. and B. L. Wanner. 2000. One-step inactivation of chromosomal genes in Escherichia coli K-12 using PCR products. Proc. Natl. Acad. Sci. USA 97: 6640- 6645.
6 Dieye, Y., J. L. Dyszel, R. Kader, and B. M. Ahmer. 2007. Systematic analysis of the regulation of type three secreted effectors in Salmonella enterica serovar Typhimurium. BMC Microbiol. 7: 3.
7 Ellermeier, C. D., J. R. Ellermeier, and J. M. Slauch. 2005. HilD, HilC and RtsA constitute a feed forward loop that controls expression of the SPI1 type three secretion system regulator hilA in Salmonella enterica serovar Typhimurium. Mol. Microbiol. 57: 691-705.
8 Ellermeier, C. D., A. Janakiraman, and J. M. Slauch. 2002. Construction of targeted single copy lac fusions using $\lambda$ Red and FLP-mediated site-specific recombination in bacteria. Gene 290: 153-161.
9 Ellermeier, J. R. and J. M. Slauch. 2007. Adaptation to the host environment: regulation of the SPI1 type III secretion system in Salmonella enterica serovar Typhimurium. Curr. Opin. Micobiol. 10: 24-29.
10 Fass, E. and E. A. Groisman. 2009. Control of Salmonella pathogenicity island-2 gene expression. Curr. Opin. Microbiol. 12: 199-204.
11 Hansen-Wester, I. and M. Hensel. 2001. Salmonella pathogenicity islands encoding type III secretion systems. Microbes Infect. 3: 549-559.
12 Haraga, A., M. B. Ohlson, and S. I. Miller. 2008. Salmonellae interplay with host cells. Nat. Rev. Microbiol. 6: 53-66.
13 Lim, S., M. Kim, J. Choi, and S. Ryu. 2010. A mutation in tdcA attenuates the virulence of Salmonella enterica serovar Typhimurium. Mol. Cells 29: 509-517.
14 Maloy, S. R., V. J. Stewart, and R. K. Taylor. 1996. Genetic analysis of pathogenic bacteria: a Laboratory Manual, Cold Spring Harbor Laboratory Press, Plainview, NY, USA
15 Merighi, M., C. D. Ellermeier, J. M. Slauch, and J. S. Gunn. 2005. Resolvase-in vivo expression technology analysis of the Salmonella enterica serovar Typhimurium PhoP and PmrA regulons in BALB/c mice. J. Bacteriol. 187: 7407- 7416.
16 Ohl, M. E. and S. I. Miller. 2001. Salmonella: a model for bacterial pathogenesis. Annu. Rev. Med. 52: 259-274.
17 Santos, R. L., R. M. Tsolis, A. J. Baumler, and L. G. Adams. 2003. Pathogenesis of Salmonella-induced enteritis. Braz. J. Med. Biol. Res. 36: 3-12.
18 Schechter, L. M. and C. A. Lee. 2001. AraC/XylS family members, HilC and HilD, directly bind and derepress the Salmonella typhimurium hilA promoter. Mol. Microbiol. 40: 1289-1299.