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Gene Review

STM2244  -  virulence protein MsgA-like protein

Salmonella enterica subsp. enterica serovar Typhimurium str. LT2

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Disease relevance of STM2244

  • A type III protein secretion system encoded by Salmonella pathogenicity island 2 (SPI2) is essential for virulence in mice, as well as survival and multiplication within macrophages [1].
  • The enteric pathogens Salmonella typhimurium and Shigella flexneri differ in most virulence attributes including infectivity, pathology and host range [2].
  • Introducing the Escherichia coli topA20::Tn10 allele to Shigella flexneri results in osmotic sensitivity, a reduced growth rate, an increase in reporter plasmid supercoiling (all common to the E. coli mutants), an inability to grow on MacConkey agar and a loss of virulence gene expression [3].
  • Marker exchange mutagenesis of horEr revealed that it encoded a regulatory protein controlling the production of antibiotic and exoenzyme virulence determinants in the phytopathogen, Erwinia carotovora subspecies carotovora [4].
  • Salmonella enterica serovar Typhimurium is lysogenized by several temperate bacteriophages that encode lysogenic conversion genes, which can act as virulence factors during infection and contribute to the genetic diversity and pathogenic potential of the lysogen [5].

High impact information on STM2244

  • The rck gene encodes a 17-kD outer membrane protein that is homologous to a family of virulence-associated outer membrane proteins, including pagC and Ail [6].
  • Mechanism of resistance to complement-mediated killing of bacteria encoded by the Salmonella typhimurium virulence plasmid gene rck [6].
  • TLR5 is a sensor for monomeric flagellin, which is a component of bacterial flagella known to be a virulence factor [7].
  • Salmonella deficient in Cu,Zn-SOD has reduced survival in macrophages and attenuated virulence in mice, which can be restored by abrogation of either the phagocyte respiratory burst or inducible nitric oxide synthase [8].
  • The results suggest that hil encodes an invasion factor or an activator of invasion factor expression. hil maps between srl and mutS near minute 59.5 of the S. typhimurium chromosome, a region adjacent to other loci that have been identified as required for S. typhimurium invasiveness and virulence [9].

Chemical compound and disease context of STM2244

  • Several loci of the SSR stimulon have been identified in Salmonella typhimurium and grouped, based on putative or known functions or products, into transport systems, C-compound catabolic enzymes, known protective enzymes, respiratory enzyme systems, regulatory proteins, virulence loci and unclassified products [10].
  • Glucose 6-phosphate dehydrogenase is required for Salmonella typhimurium virulence and resistance to reactive oxygen and nitrogen intermediates [11].
  • The lipopolysaccharide (LPS) structure of Salmonella typhimurium has been correlated with the virulence of wild-type strain LT2 [12].
  • The glucan-binding domain (GLU) of the enzyme glucosyltransferase (GTF), which is an important virulence factor of Streptococcus mutans, was recombinantly expressed in the insoluble phase in S. enterica serovar Typhimurium, and the immunogenicity of this construct was studied in mice [13].
  • The spv virulence operon of Salmonella typhimurium LT2 is regulated negatively by the cyclic AMP (cAMP)-cAMP receptor protein system [14].

Biological context of STM2244

  • The traJ gene of the virulence plasmid of Salmonella enterica serovar Typhimurium (pSLT) encodes a transcriptional activator of the transfer operon [15].
  • These data show that overexpression of the S. flexneri topoisomerase IV genes can compensate for the loss of topoisomerase I in terms of general viability of the cell, DNA supercoiling, and (partially) virulence gene expression [3].
  • Collectively, these results suggest that sifA arose by horizontal gene transfer into Salmonella and its product is involved in a virulence-associated intracellular phenotype related to Salmonella-induced filament formation [16].
  • Sequence analysis of the rap gene revealed a predicted protein product showing strong homology to SlyA, originally thought to be a haemolytic virulence determinant in Salmonella typhimurium [4].
  • Recently, by hybridizing an E. coli K-12 gene array with cDNA synthesized from RNA extracted from EHEC strain 86-24 and its isogenic luxS mutant, we observed that other potential virulence-associated factors, such as genes encoding the expression and assembly of flagella, motility and chemotaxis, were also activated by quorum sensing [17].

Anatomical context of STM2244

  • Identification of a Salmonella virulence gene required for formation of filamentous structures containing lysosomal membrane glycoproteins within epithelial cells [16].
  • Typhimurium is attenuated for virulence after oral infection of immunocompromised gp91phox(-/-) mice that lack a functional NADPH phagocyte oxidase, suggesting that sigma(E) plays an important role in resistance to non-oxidative mucosal host defences such as anti-microbial peptides [18].
  • This survival requires coordinate transcriptional activation of virulence genes within acidified macrophage phagosomes [19].
  • Neutrophil depletion by antibody treatment of mice did not restore the virulence of SPI2 or auxotrophic mutant strains, supporting the hypothesis that attenuation of the strains is not due to greater susceptibility to neutrophil killing [20].
  • Subsequently, the virulence potential of this mutant was examined in a cell culture system using T84 intestinal epithelial and RAW264.7 macrophage cell lines and a mouse model of salmonellosis [21].

Associations of STM2244 with chemical compounds

  • Optimal conjugation frequency requires filter matings on M9 minimal glucose plates with a recipient strain lacking the virulence plasmid [22].
  • Although most mutations in SPI2 lead to a strong reduction of virulence, they have different effects in vitro, with some mutants having significantly increased sensitivity to gentamicin and the antibacterial peptide polymyxin B [23].
  • Both these chromosomal fragments, whose presence is correlated with serogroups O1 and O2 and to the virulence of APEC strains belonging to these serogroups, are good candidates for being part of novel virulence determinants of APEC [24].
  • The present study examined the effects of pH, carbohydrate sources, amino acids and lactate on expression of Salm. enteritidis virulence by measuring expression of hilA [25].

Regulatory relationships of STM2244

  • Modulation of hilA by counteracting repressing and derepressing mechanisms may allow Salmonella serovar Typhimurium to regulate its virulence genes in response to different situations in vivo [26].
  • The observation of pmrH and pagP expression in the intestine refutes the paradigm of PhoP/PhoQ and PmrA/PmrB in vivo expression as solely intracellularly induced and supports previous data demonstrating peroral virulence attenuation of pmrH mutants [27].

Other interactions of STM2244

  • These data are consistent with spvR being poorly transcribed from the single-copy virulence plasmid in S. typhimurium LT2 and with a suppression of this defect via inactivation of the cAMP-CRP system [14].
  • By using a lacZ reporter transcriptional fusion to the spvB structural gene on the single-copy virulence plasmid, it was found that while spvB transcription was induced in stationary-phase cultures, the induced level of expression was lower than that reported for the spv system in other serovars of Salmonella [14].
  • The gene (tlpA) encoding this protein (TlpA) was isolated from the large virulence-associated plasmid of S. typhimurium and sequenced in order to predict the primary structure of TlpA. tlpA encodes a 371-amino acid soluble protein with a calculated M(r) of 41600 and pI of 4.63 [28].
  • hilA encodes an activator of Salmonella enterica serovar Typhimurium virulence genes and is transcriptionally modulated by environmental conditions [26].
  • All but the ptsC and rfaY mutants were attenuated for virulence [29].

Analytical, diagnostic and therapeutic context of STM2244

  • Although the disease progression is slower, S. typhimurium mutS recD mutants retain the ability to cause lethal infections, and, thus, hybrids constructed in mutS recD hosts may permit the analysis of virulence factors in a surrogate animal model [30].
  • Reduced or increased numbers of CFU and increased spleen size in the principal groups of mice relative to that of the nonvaccinated control group were considered protectiveness or virulence (survival) criteria [31].
  • Therefore, a DNA microarray chip of 71 virulence genes of S. typhimurium was developed and evaluated using 10 isolates [32].
  • In order to design and validate a method to identify virulence genes of Salmonella typhimurium using DNA microarray, a protocol was developed to label the isolated bacterial DNA directly and to use PCR amplification of limited numbers of genes to validate the hybridization signals [32].
  • The specificity of cross protection was studied using S. typhimurium, Salmonella enteritidis and Salmonella dublin for vaccination and challenge, including challenge with variants of S. typhimurium and S. enteritidis of similar virulence which differed in the main LPS (lipopolysaccharide) antigen (0-4 or 0-9) [33].


  1. Salmonella pathogenicity island 2 mediates protection of intracellular Salmonella from reactive nitrogen intermediates. Chakravortty, D., Hansen-Wester, I., Hensel, M. J. Exp. Med. (2002) [Pubmed]
  2. Cognate gene clusters govern invasion of host epithelial cells by Salmonella typhimurium and Shigella flexneri. Groisman, E.A., Ochman, H. EMBO J. (1993) [Pubmed]
  3. Overexpression of the Shigella flexneri genes coding for DNA topoisomerase IV compensates for loss of DNA topoisomerase I: effect on virulence gene expression. McNairn, E., Ni Bhriain, N., Dorman, C.J. Mol. Microbiol. (1995) [Pubmed]
  4. The rap and hor proteins of Erwinia, Serratia and Yersinia: a novel subgroup in a growing superfamily of proteins regulating diverse physiological processes in bacterial pathogens. Thomson, N.R., Cox, A., Bycroft, B.W., Stewart, G.S., Williams, P., Salmond, G.P. Mol. Microbiol. (1997) [Pubmed]
  5. Genetic and molecular analysis of GogB, a phage-encoded type III-secreted substrate in Salmonella enterica serovar typhimurium with autonomous expression from its associated phage. Coombes, B.K., Wickham, M.E., Brown, N.F., Lemire, S., Bossi, L., Hsiao, W.W., Brinkman, F.S., Finlay, B.B. J. Mol. Biol. (2005) [Pubmed]
  6. Mechanism of resistance to complement-mediated killing of bacteria encoded by the Salmonella typhimurium virulence plasmid gene rck. Heffernan, E.J., Reed, S., Hackett, J., Fierer, J., Roudier, C., Guiney, D. J. Clin. Invest. (1992) [Pubmed]
  7. Involvement of Toll-like receptor 5 in the recognition of flagellated bacteria. Feuillet, V., Medjane, S., Mondor, I., Demaria, O., Pagni, P.P., Galán, J.E., Flavell, R.A., Alexopoulou, L. Proc. Natl. Acad. Sci. U.S.A. (2006) [Pubmed]
  8. Periplasmic superoxide dismutase protects Salmonella from products of phagocyte NADPH-oxidase and nitric oxide synthase. De Groote, M.A., Ochsner, U.A., Shiloh, M.U., Nathan, C., McCord, J.M., Dinauer, M.C., Libby, S.J., Vazquez-Torres, A., Xu, Y., Fang, F.C. Proc. Natl. Acad. Sci. U.S.A. (1997) [Pubmed]
  9. Identification of a Salmonella typhimurium invasion locus by selection for hyperinvasive mutants. Lee, C.A., Jones, B.D., Falkow, S. Proc. Natl. Acad. Sci. U.S.A. (1992) [Pubmed]
  10. The starvation-stress response (SSR) of Salmonella. Spector, M.P. Adv. Microb. Physiol. (1998) [Pubmed]
  11. Glucose 6-phosphate dehydrogenase is required for Salmonella typhimurium virulence and resistance to reactive oxygen and nitrogen intermediates. Lundberg, B.E., Wolf, R.E., Dinauer, M.C., Xu, Y., Fang, F.C. Infect. Immun. (1999) [Pubmed]
  12. The polysaccharide portion of lipopolysaccharide regulates antigen-specific T-cell activation via effects on macrophage-mediated antigen processing. Zirk, N.M., Hashmi, S.F., Ziegler, H.K. Infect. Immun. (1999) [Pubmed]
  13. Effect of attenuated Salmonella enterica serovar Typhimurium expressing a Streptococcus mutans antigen on secondary responses to the cloned protein. Jespersgaard, C., Zhang, P., Hajishengallis, G., Russell, M.W., Michalek, S.M. Infect. Immun. (2001) [Pubmed]
  14. The spv virulence operon of Salmonella typhimurium LT2 is regulated negatively by the cyclic AMP (cAMP)-cAMP receptor protein system. O'Byrne, C.P., Dorman, C.J. J. Bacteriol. (1994) [Pubmed]
  15. Regulation of traJ transcription in the Salmonella virulence plasmid by strand-specific DNA adenine hemimethylation. Camacho, E.M., Casadesús, J. Mol. Microbiol. (2005) [Pubmed]
  16. Identification of a Salmonella virulence gene required for formation of filamentous structures containing lysosomal membrane glycoproteins within epithelial cells. Stein, M.A., Leung, K.Y., Zwick, M., Garcia-del Portillo, F., Finlay, B.B. Mol. Microbiol. (1996) [Pubmed]
  17. Quorum sensing Escherichia coli regulators B and C (QseBC): a novel two-component regulatory system involved in the regulation of flagella and motility by quorum sensing in E. coli. Sperandio, V., Torres, A.G., Kaper, J.B. Mol. Microbiol. (2002) [Pubmed]
  18. The alternative sigma factor sigma is required for resistance of Salmonella enterica serovar Typhimurium to anti-microbial peptides. Crouch, M.L., Becker, L.A., Bang, I.S., Tanabe, H., Ouellette, A.J., Fang, F.C. Mol. Microbiol. (2005) [Pubmed]
  19. Further characterization of the PhoP regulon: identification of new PhoP-activated virulence loci. Belden, W.J., Miller, S.I. Infect. Immun. (1994) [Pubmed]
  20. Role of neutrophils in murine salmonellosis. Cheminay, C., Chakravortty, D., Hensel, M. Infect. Immun. (2004) [Pubmed]
  21. The two murein lipoproteins of Salmonella enterica serovar Typhimurium contribute to the virulence of the organism. Sha, J., Fadl, A.A., Klimpel, G.R., Niesel, D.W., Popov, V.L., Chopra, A.K. Infect. Immun. (2004) [Pubmed]
  22. The virulence plasmid of Salmonella typhimurium is self-transmissible. Ahmer, B.M., Tran, M., Heffron, F. J. Bacteriol. (1999) [Pubmed]
  23. Mutations in Salmonella pathogenicity island 2 (SPI2) genes affecting transcription of SPI1 genes and resistance to antimicrobial agents. Deiwick, J., Nikolaus, T., Shea, J.E., Gleeson, C., Holden, D.W., Hensel, M. J. Bacteriol. (1998) [Pubmed]
  24. Genomic subtraction for the identification of putative new virulence factors of an avian pathogenic Escherichia coli strain of O2 serogroup. Schouler, C., Koffmann, F., Amory, C., Leroy-Sétrin, S., Moulin-Schouleur, M. Microbiology (Reading, Engl.) (2004) [Pubmed]
  25. Expression of the hilA Salmonella typhimurium gene in a poultry Salm. enteritidis isolate in response to lactate and nutrients. Durant, J.A., Corrier, D.E., Stanker, L.H., Ricke, S.C. J. Appl. Microbiol. (2000) [Pubmed]
  26. The small nucleoid-binding proteins H-NS, HU, and Fis affect hilA expression in Salmonella enterica serovar Typhimurium. Schechter, L.M., Jain, S., Akbar, S., Lee, C.A. Infect. Immun. (2003) [Pubmed]
  27. Resolvase-in vivo expression technology analysis of the Salmonella enterica serovar Typhimurium PhoP and PmrA regulons in BALB/c mice. Merighi, M., Ellermeier, C.D., Slauch, J.M., Gunn, J.S. J. Bacteriol. (2005) [Pubmed]
  28. A new alpha-helical coiled coil protein encoded by the Salmonella typhimurium virulence plasmid. Koski, P., Saarilahti, H., Sukupolvi, S., Taira, S., Riikonen, P., Osterlund, K., Hurme, R., Rhen, M. J. Biol. Chem. (1992) [Pubmed]
  29. Identification of Salmonella typhimurium genes required for colonization of the chicken alimentary tract and for virulence in newly hatched chicks. Turner, A.K., Lovell, M.A., Hulme, S.D., Zhang-Barber, L., Barrow, P.A. Infect. Immun. (1998) [Pubmed]
  30. Effect of mutS and recD mutations on Salmonella virulence. Zahrt, T.C., Buchmeier, N., Maloy, S. Infect. Immun. (1999) [Pubmed]
  31. Variation of Brucella abortus 2308 infection in BALB/c mice induced by prior vaccination with salt-extractable periplasmic proteins from Brucella abortus 19. Pugh, G.W., Tabatabai, L.B. Infect. Immun. (1996) [Pubmed]
  32. Using PCR amplification to increase the confidence level of Salmonella typhimurium DNA microarray chip hybridization. Courtney, S., Mossoba, M.E., Hammack, T.S., Keys, C., Al-Khaldi, S.F. Mol. Cell. Probes (2006) [Pubmed]
  33. Immunity induced by live attenuated Salmonella vaccines. Hormaeche, C.E., Joysey, H.S., Desilva, L., Izhar, M., Stocker, B.A. Res. Microbiol. (1990) [Pubmed]
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