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Chapter 12 : Virulence Gene Clusters and Putative Pathogenicity Islands in Listeriae

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Virulence Gene Clusters and Putative Pathogenicity Islands in Listeriae, Page 1 of 2

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Abstract:

The genus comprises six characterized species, , , , , , and . It was therefore surprising to find in a gene cluster highly reminiscent of the virulence gene cluster of the two pathogenic species. This gene cluster is also located at the same position on the chromosome of as the virulence gene clusters of and . The gene cluster is, however, substantially larger than those of the pathogenic species and contains three additional ORFs, which, based on their flanking regulatory features, represent potentially transcribed genes. The conversion of the -type gene cluster to the virulence gene clusters of and probably would have involved the removal of all unnecessary genes and the optimization of the expression of these genes in a mammalian cell. The generation of gene "lean" virulence gene cluster, stably anchored in the bacterial chromosome, may thus represent the ultimate outcome in the evolution of what is called today a pathogenicity island (PAI). During a systemic infection, has to cross several tissue barriers which consist of different cell types. Today's knowledge of the genetics of the pathogenic species, and , and its comparison with that of the nonpathogenic species and , suggests a stepwise acquisition of virulence genes which may have occurred by common as well as species-specific mechanisms.

Citation: Eva Ng J, Goebel W, Vázquez-Boland J. 1999. Virulence Gene Clusters and Putative Pathogenicity Islands in Listeriae, p 219-232. In Kaper J, Hacker J (ed), Pathogenicity Islands and Other Mobile Virulence Elements. ASM Press, Washington, DC. doi: 10.1128/9781555818173.ch12

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Figures

Image of Figure 1
Figure 1

Schematic representation of the Prfa-dependent virulence gene clusters of listeriae. The direction of transcription is indicated by arrows; in it is identical to that in . Note that in and , the product of stimulates the transcription of the bicistronic mRNA; in this autoregulatory loop is interrupted by the divergently transcribed ORFE. The sequences for and have not yet been completely determined. For and , the presence of sequences homologous to ORFB and ORFA has been shown by DNA hybridization ( ); the sequence has not yet been determined. For further details and references, see the text.

Citation: Eva Ng J, Goebel W, Vázquez-Boland J. 1999. Virulence Gene Clusters and Putative Pathogenicity Islands in Listeriae, p 219-232. In Kaper J, Hacker J (ed), Pathogenicity Islands and Other Mobile Virulence Elements. ASM Press, Washington, DC. doi: 10.1128/9781555818173.ch12
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Image of Figure 2
Figure 2

Schematic representation of internalin genes and their genetic context. (A) Large internalins of . was generated by a deletion of the C terminus of and the N terminus of . (B) Small internalins: of and of . PB, PrfA-box. For further details see the text. Additional small internalins of are shown in Fig. 3 .

Citation: Eva Ng J, Goebel W, Vázquez-Boland J. 1999. Virulence Gene Clusters and Putative Pathogenicity Islands in Listeriae, p 219-232. In Kaper J, Hacker J (ed), Pathogenicity Islands and Other Mobile Virulence Elements. ASM Press, Washington, DC. doi: 10.1128/9781555818173.ch12
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Image of Figure 3
Figure 3

Schematic representation of the known genes of the -specific virulence locus. The direction of transcription is indicated by arrows. PB, PrfA box; Ter, transcriptional terminator. The sphingomyelinase gene () is PrfA independent.

Citation: Eva Ng J, Goebel W, Vázquez-Boland J. 1999. Virulence Gene Clusters and Putative Pathogenicity Islands in Listeriae, p 219-232. In Kaper J, Hacker J (ed), Pathogenicity Islands and Other Mobile Virulence Elements. ASM Press, Washington, DC. doi: 10.1128/9781555818173.ch12
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