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Gene Review

ipaB  -  invasion protein

Shigella flexneri 5a str. M90T

 
 
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Disease relevance of ipaB

 

High impact information on ipaB

  • In mutants of some genes encoding the secretion machinery the organelle was absent, whereas ipaB and ipaC mutants displayed normal secretons [2].
  • Deletion mutants in the invasion invasion plasmid antigen B (ipaB) of Shigella flexneri are not cytotoxic [3].
  • The consequence of the inactivation of ipaB on the intracellular behaviour of S.flexneri was investigated using the macrophage cell line J774 [4].
  • By creating mutations within the Shigella flexneri ipaB gene, we have demonstrated that the invasion of epithelial cells is a three-step process encompassing adhesion on the cell surface, entry and lysis of the phagocytic vacuole allowing subsequent access to the cytoplasm [4].
  • Complete DNA sequences of ipaB, -C, and -D were determined [5].
 

Biological context of ipaB

  • The nucleotide sequence revealed that in addition to the ipaB and ipaC genes encoding polypeptides b and c, a third complete open reading frame was found within the fragment [1].
  • These results demonstrate that ipaB is essential for S. flexneri to induce apoptosis in macrophages [6].
  • To address the role of the ipa genes, which are clustered in an operon, we constructed a selectable cassette that does not affect transcription of downstream genes and used this cassette to inactivate the ipaB, ipaC, and ipaD genes [7].
  • Analysis of rRNA gene restriction patterns (ribotype) showed that the environmental isolates shared ribotypes with a collection of clinical isolates, but in contrast to the clinical isolates, 10 of the 11 environmental isolates were either negative or carried deletions in the plasmid-encoded invasion-associated genes ipaB, ipaC, and ipaD [8].
  • The ipaB gene of Shigella flexneri and macrophage-programmed cell death [9].
 

Associations of ipaB with chemical compounds

  • Cultures grown to stationary phase in the presence of Congo red contain extracellular filaments whose composition and morphology are similar to those produced by the hypersecreting ipaB and ipaD mutants [10].
  • Challenge with a noninvasive ipaB mutant strain resulted in the induction of a similar, but less intense, profile of phosphotyrosine-containing host cell proteins [11].
 

Other interactions of ipaB

  • Genes ipaB, ipaC and ipaD mapped to contiguous 4.6-kilobase (kb) and 1.0-kb HindIII fragments contained within a larger (23-kb) BamHI fragment [12].
  • An increase in the copy number of invE enhanced the expression of ipaB and invJ in the absence of virF [13].
  • The S. flexneri cytotoxic genes have been localized to the ipa operon of shigella's virulence plasmid. ipaB, C and D deletion mutants are not invasive and therefore not cytotoxic [6].
 

Analytical, diagnostic and therapeutic context of ipaB

  • Western blot (immunoblot) and Southern hybridization analyses indicated that one of the fusions was located in a known inv gene, ipaB, which encodes one of the major immunogenic peptides of Shigella spp [14].

References

  1. Nucleotide sequence of the invasion plasmid antigen B and C genes (ipaB and ipaC) of Shigella flexneri. Baudry, B., Kaczorek, M., Sansonetti, P.J. Microb. Pathog. (1988) [Pubmed]
  2. The tripartite type III secreton of Shigella flexneri inserts IpaB and IpaC into host membranes. Blocker, A., Gounon, P., Larquet, E., Niebuhr, K., Cabiaux, V., Parsot, C., Sansonetti, P. J. Cell Biol. (1999) [Pubmed]
  3. A bacterial invasin induces macrophage apoptosis by binding directly to ICE. Chen, Y., Smith, M.R., Thirumalai, K., Zychlinsky, A. EMBO J. (1996) [Pubmed]
  4. IpaB of Shigella flexneri causes entry into epithelial cells and escape from the phagocytic vacuole. High, N., Mounier, J., Prévost, M.C., Sansonetti, P.J. EMBO J. (1992) [Pubmed]
  5. Characterization of invasion plasmid antigen genes (ipaBCD) from Shigella flexneri. Venkatesan, M.M., Buysse, J.M., Kopecko, D.J. Proc. Natl. Acad. Sci. U.S.A. (1988) [Pubmed]
  6. IpaB mediates macrophage apoptosis induced by Shigella flexneri. Zychlinsky, A., Kenny, B., Ménard, R., Prévost, M.C., Holland, I.B., Sansonetti, P.J. Mol. Microbiol. (1994) [Pubmed]
  7. Nonpolar mutagenesis of the ipa genes defines IpaB, IpaC, and IpaD as effectors of Shigella flexneri entry into epithelial cells. Ménard, R., Sansonetti, P.J., Parsot, C. J. Bacteriol. (1993) [Pubmed]
  8. Isolation of Shigella dysenteriae type 1 and S. flexneri strains from surface waters in Bangladesh: comparative molecular analysis of environmental Shigella isolates versus clinical strains. Faruque, S.M., Khan, R., Kamruzzaman, M., Yamasaki, S., Ahmad, Q.S., Azim, T., Nair, G.B., Takeda, Y., Sack, D.A. Appl. Environ. Microbiol. (2002) [Pubmed]
  9. The ipaB gene of Shigella flexneri and macrophage-programmed cell death. Zychlinsky, A., Kenny, B., Prevost, M.C., Holland, I.B., Sansonetti, P.J. Infectious agents and disease. (1993) [Pubmed]
  10. Enhanced secretion through the Shigella flexneri Mxi-Spa translocon leads to assembly of extracellular proteins into macromolecular structures. Parsot, C., Ménard, R., Gounon, P., Sansonetti, P.J. Mol. Microbiol. (1995) [Pubmed]
  11. Shigella flexneri-HeLa cell interactions: a putative role for host cell protein kinases. Collaco, C., Dyer, R.B., Doan, R., Herzog, N.K., Niesel, D.W. FEMS Immunol. Med. Microbiol. (1995) [Pubmed]
  12. Molecular cloning of invasion plasmid antigen (ipa) genes from Shigella flexneri: analysis of ipa gene products and genetic mapping. Buysse, J.M., Stover, C.K., Oaks, E.V., Venkatesan, M., Kopecko, D.J. J. Bacteriol. (1987) [Pubmed]
  13. Genetic analysis of an invasion region by use of a Tn3-lac transposon and identification of a second positive regulator gene, invE, for cell invasion of Shigella sonnei: significant homology of invE with ParB of plasmid P1. Watanabe, H., Arakawa, E., Ito, K., Kato, J., Nakamura, A. J. Bacteriol. (1990) [Pubmed]
  14. Identification of Shigella invasion genes by isolation of temperature-regulated inv::lacZ operon fusions. Hromockyj, A.E., Maurelli, A.T. Infect. Immun. (1989) [Pubmed]
 
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