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Chapter 9 : Adhesion-Dependent Upregulation of Bacterial Genes

Authors: Itzhak Ofek, David L. Hasty, Ron J. Doyle
Content Type: Monograph
Publication Year: 2003

Category: Bacterial Pathogenesis

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Abstract:

There are many studies showing upregulation of genes in vivo. Whether adhesion is required for the activation of many these genes is not known. In a few cases, however, it has been shown that adhesion itself activates gene expression. The PilC1-mediated contact then activates the contact regulatory element of (CREN) site within the promoter, which induces expression of bacterial genes for a second stage of the process. In this step, more PilC1 adhesin molecules are expressed, eventually leading to the presentation of PilC1 adhesin at the pilus tip. This step is followed by upregulation of the machinery for intimate attachment associated with attaching/effacing lesions and concomitant downregulation of pilus expression. A CREN-like element also participates in the intimate-adhesion step of the process. It appears that the Opc and Opa proteins may also be involved in some aspects of the adhesion process. The target cell receptor involved in PilC1-mediated adhesion is the CD46 glycoprotein. That the outer membrane form of PilC1 could mediate adhesion in vitro was shown by centrifuging nonpiliated bacteria onto epithelial cells. The few examples provided in this chapter show that this phenomenon does occur, but the true extent to which the process of adhesion activates bacterial gene expression remains to be more fully explored.

Citation: Ofek I, Hasty D, Doyle R. 2003. Adhesion-Dependent Upregulation of Bacterial Genes, p 143-146. In Bacterial Adhesion to Animal Cells and Tissues. ASM Press, Washington, DC. doi: 10.1128/9781555817800.ch9
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Adhesion-Dependent Upregulation of Bacterial Genes
Citation: Ofek I, Hasty D, Doyle R. 2003. Adhesion-Dependent Upregulation of Bacterial Genes, p 143-146. In Bacterial Adhesion to Animal Cells and Tissues. ASM Press, Washington, DC. doi: 10.1128/9781555817800.ch9
/content/10.1128/9781555817800.chap9.fig9-1
FIGURE 9.1

Schematic presentation of the effect of PapG-mediated adhesion on the expression of bacterial genes, exemplified by uropathogenic bound to host cells. On contact with epithelial cells, a number of bacterial genes become upregulated; this, in turn, may either downregulate or upregulate the expression of other genes. It has been shown that PapG-mediated adhesion of uropathogenic causes upregulation of the gene, which is involved in the regulation of iron acquisition.

10.1128/9781555817800/fig9-1_thmb.gif
10.1128/9781555817800/fig9-1.gif
Image of FIGURE 9.1
FIGURE 9.1

Schematic presentation of the effect of PapG-mediated adhesion on the expression of bacterial genes, exemplified by uropathogenic bound to host cells. On contact with epithelial cells, a number of bacterial genes become upregulated; this, in turn, may either downregulate or upregulate the expression of other genes. It has been shown that PapG-mediated adhesion of uropathogenic causes upregulation of the gene, which is involved in the regulation of iron acquisition.

Citation: Ofek I, Hasty D, Doyle R. 2003. Adhesion-Dependent Upregulation of Bacterial Genes, p 143-146. In Bacterial Adhesion to Animal Cells and Tissues. ASM Press, Washington, DC. doi: 10.1128/9781555817800.ch9
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FIGURE 9.2

Schematic presentation of the effect of PilC-mediated adhesion on the expression of bacterial genes, exemplified by bound to host cells. As with uropathogenic on contact of with epithelial cells, a number of genes become upregulated; this may either downregulate or upregulate the expression of other genes. In this example, PilC1-mediated initial adhesion of is a signal that induces the expression of and genes. Once induced, CrgA downregulates capsule, pili, and itself and upregulates the expression of as yet unidentified genes involved in intimate adhesion.

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10.1128/9781555817800/fig9-2.gif
Image of FIGURE 9.2
FIGURE 9.2

Schematic presentation of the effect of PilC-mediated adhesion on the expression of bacterial genes, exemplified by bound to host cells. As with uropathogenic on contact of with epithelial cells, a number of genes become upregulated; this may either downregulate or upregulate the expression of other genes. In this example, PilC1-mediated initial adhesion of is a signal that induces the expression of and genes. Once induced, CrgA downregulates capsule, pili, and itself and upregulates the expression of as yet unidentified genes involved in intimate adhesion.

Citation: Ofek I, Hasty D, Doyle R. 2003. Adhesion-Dependent Upregulation of Bacterial Genes, p 143-146. In Bacterial Adhesion to Animal Cells and Tissues. ASM Press, Washington, DC. doi: 10.1128/9781555817800.ch9
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Download as Powerpoint
/content/10.1128/9781555817800.chap9.fig9-3
FIGURE 9.3

Schematic presentation of the effect of YadA-mediated adhesion on the expression of bacterial genes, exemplified by bound to host cells. As with uropathogenic and on contact with epithelial cells, a number of genes become upregulated; this may either upregulate or downregulate the expression of other genes. YadA/invasin-mediated adhesion of causes YopN to open the translocation pore and release the negative regulator YscM, which leads to increased expression of genes and other genes of the type III secretion system and translocation of Yop effector proteins into the host cell.

10.1128/9781555817800/fig9-3_thmb.gif
10.1128/9781555817800/fig9-3.gif
Image of FIGURE 9.3
FIGURE 9.3

Schematic presentation of the effect of YadA-mediated adhesion on the expression of bacterial genes, exemplified by bound to host cells. As with uropathogenic and on contact with epithelial cells, a number of genes become upregulated; this may either upregulate or downregulate the expression of other genes. YadA/invasin-mediated adhesion of causes YopN to open the translocation pore and release the negative regulator YscM, which leads to increased expression of genes and other genes of the type III secretion system and translocation of Yop effector proteins into the host cell.

Citation: Ofek I, Hasty D, Doyle R. 2003. Adhesion-Dependent Upregulation of Bacterial Genes, p 143-146. In Bacterial Adhesion to Animal Cells and Tissues. ASM Press, Washington, DC. doi: 10.1128/9781555817800.ch9
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References

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1. Boyd, A. P.,, N. Grosdent,, S. Totemeyer,, C. Geuijen,, S. Bleves,, M. Iriarte,, I. Lambermont,, J. N. Octave,, and G. R. Cornelis. 2000. Yersinia enterocolitica can deliver Yop proteins into a wide range of cell types: development of a delivery system for heterologous proteins. Eur. J. Cell Biol. 79: 659– 671.
2. Cornelis, G. 1997. Contact with eukaryotic cells: a new signal triggering bacterial gene expression. Trends Microbiol. 5: 43– 45.
3. Cornelis, G. 2002. The Yersinia Ysc-YOP ‘type III’ weaponry. Nat. Rev. Mol. Cell Biol. 3: 742– 752.
4. Kallström, H.,, M. K. Liszewski,, J. P. Atkinson,, and A. B. Jonsson. 1997. Membrane cofactor protein (MCP or CD46) is a cellular pilus receptor for pathogenic Neisseria. Mol. Microbiol. 25: 639– 647.
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8. Rahman, M.,, H. Källström,, S. Normark,, and A.-B. Jonsson. 1997. PilC of pathogenic Neisseria is associated with the bacterial cell surface. Mol. Microbiol. 25: 11– 25.
9. Rosqvist, R.,, K. E. Magnusson,, and H. Wolf-Watz. 1994. Target cell contact triggers expression and polarized transfer of Yersinia YopE cytotoxin into mammalian cells. EMBO J. 13: 964– 972.
10. Taha, M.-K., 2002. Transcriptional regulation of meningococcal gene expression upon adhesion to target cells, p. 165– 182. In M. Wilson, (ed.), Bacterial Adhesion to Host Cells. Cambridge University Press, Cambridge, United Kingdom.
11. Taha, M.-K.,, P. C. Morand,, Y. Pereira,, E. Eugène,, D. Giorgini,, M. Larribe,, and X. Nassif. 1998. Pilus-mediated adhesion of Neisseria meningitidis: the essential role of cell contactdependent transcriptional upregulation of the PilC1 protein. Mol. Microbiol. 28: 1153– 1163.
12. Zhang, J. P.,, and S. Normark. 1996. Induction of gene expression in Escherichia coli after pilus-mediated adherence. Science 273: 1234– 1236.

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