1887

Chapter 16 : Gene Associations in Bacterial Pathogenesis: Pathogenicity Islands and Genomic Deletions

MyBook is a cheap paperback edition of the original book and will be sold at uniform, low price.

Ebook: Choose a downloadable PDF or ePub file. Chapter is a downloadable PDF file. File must be downloaded within 48 hours of purchase

Buy this Chapter
Digital (?) $30.00

Preview this chapter:
Zoom in
Zoomout

Gene Associations in Bacterial Pathogenesis: Pathogenicity Islands and Genomic Deletions, Page 1 of 2

| /docserver/preview/fulltext/10.1128/9781555817749/9781555812713_Chap16-1.gif /docserver/preview/fulltext/10.1128/9781555817749/9781555812713_Chap16-2.gif

Abstract:

This chapter examines how bacteria have altered their genome content to better survive and replicate within a disease environment. It specifically examines two of the latter evolutionary pathways and their relationship to the development of bacterial pathogenesis: (i) gene acquisition and (ii) gene deletion. Pathogenicity islands are perfect examples of how gene acquisition by horizontal transfer can generate sequence diversity in bacterial pathogens and enable them to evolve new virulence traits. As a pathogenic bacterium, can serve as a useful model in understanding the evolution of bacteria toward an obligate intracellular lifestyle. Researchers have elegantly reviewed the processes that contribute to the evolution of bacterial genomes, and their findings are used to summarize and bring perspective to the gene associations in bacterial pathogenesis. Pathogenicity islands and their associated genes, such as type III secretion systems, demonstrate how many bacterial species have acquired and evolved virulence functions using the same basic mechanism of horizontal gene transfer followed by mutation and adaptation to the lifestyle of the host bacterium. The insertion and deletion of pathogenicity islands as complete blocks of genes suggest that they may act as discrete molecular units within the genome of bacterial pathogens. Naturally competent bacterial species demonstrate many instances of sequence variation which have resulted from the recombination of small DNA fragments within genes. This provides another mechanism by which pathogens may evolve virulence functions with a good example being the evolution of penicillin-binding proteins in .

Citation: Mahenthiralingam E. 2004. Gene Associations in Bacterial Pathogenesis: Pathogenicity Islands and Genomic Deletions, p 249-274. In Miller R, Day M (ed), Microbial Evolution. ASM Press, Washington, DC. doi: 10.1128/9781555817749.ch16
Highlighted Text: Show | Hide
Loading full text...

Full text loading...

Figures

Image of FIGURE 1
FIGURE 1

Concepts of pathogen-host interactions in bacterial infectious diseases. Definition of commensal bacteria, opportunistic pathogens, primary pathogens, and host organism are illustrated in relation to disease and pathogenicity. The relationship between each class of bacteria and the colonized host organism is indicated by the arrows. Definitions are drawn from .

Citation: Mahenthiralingam E. 2004. Gene Associations in Bacterial Pathogenesis: Pathogenicity Islands and Genomic Deletions, p 249-274. In Miller R, Day M (ed), Microbial Evolution. ASM Press, Washington, DC. doi: 10.1128/9781555817749.ch16
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of FIGURE 2
FIGURE 2

The concepts that define a bacterial pathogenicity island. A model pathogenicity island is illustrated using the criteria described in the text. The PAI (large grey box) is embedded within an area of core genome (black line). Genes and features characteristic of PAIs are indicated by the arrows, and a brief explanation of each defining feature is provided in the text boxes.

Citation: Mahenthiralingam E. 2004. Gene Associations in Bacterial Pathogenesis: Pathogenicity Islands and Genomic Deletions, p 249-274. In Miller R, Day M (ed), Microbial Evolution. ASM Press, Washington, DC. doi: 10.1128/9781555817749.ch16
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of FIGURE 3
FIGURE 3

Distribution of PAIs in serovar Typhi. The large black circle represents the circular chromosome of serovar Typhi. The relative position of each PAI to base zero is indicated by the arrows and linked to a text box providing the name and pertinent features of each PAI. The data presented were adapted from or retrieved from the genome sequence file, GenBank accession no. AL513382.

Citation: Mahenthiralingam E. 2004. Gene Associations in Bacterial Pathogenesis: Pathogenicity Islands and Genomic Deletions, p 249-274. In Miller R, Day M (ed), Microbial Evolution. ASM Press, Washington, DC. doi: 10.1128/9781555817749.ch16
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of FIGURE 4
FIGURE 4

G + C content of serovar Typhi PAIs 2 and 9 (SPI-2 and SPI-9). Annotated genome sequence data (GenBank accession no AL513382) was viewed using the computer program Artemis ( ). Each plot shows the encoded genes and G + C content of the genomic region (indicated on the right of the figure). The low G+C content (typical for most PAI) of SPI-2 is shown in A. In addition, SPI-2 demonstrates a mosaic structure with G + C content at the 3' end of the PAI, carrying tetrathionate genes, similar to the genome average. The atypical high G + C content of SPI-9 is shown in B; the lysogenic phage inserted adjacent to SPI-9 is also shown.

Citation: Mahenthiralingam E. 2004. Gene Associations in Bacterial Pathogenesis: Pathogenicity Islands and Genomic Deletions, p 249-274. In Miller R, Day M (ed), Microbial Evolution. ASM Press, Washington, DC. doi: 10.1128/9781555817749.ch16
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of FIGURE 5
FIGURE 5

Gene order and organization of the type III secretion system of encoded on plasmid pCD1. (A) A model of the type III secretion system is shown spanning the inner and outer bacterial membranes and inserting into the cytoplasmic membrane of a host cell (the macrophage). Component proteins for each membrane domain are indicated and correspond to the gene names shown in ?. (B) The genes encoding the major components of the type III secretion are shown as arrows indicating their direction of transcription. Shaded arrows indicate individual genes drawn as a single cluster for the purposes of the figure. Genes that are homologous to those which encode the gram-negative flagellum basal body are shown.

Citation: Mahenthiralingam E. 2004. Gene Associations in Bacterial Pathogenesis: Pathogenicity Islands and Genomic Deletions, p 249-274. In Miller R, Day M (ed), Microbial Evolution. ASM Press, Washington, DC. doi: 10.1128/9781555817749.ch16
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of FIGURE 6
FIGURE 6

Horizontally acquired virulence factors that contribute to the pathogenesis of enterohemorrhagic O157:H7. Virulence genes and their location are shown by the open blocks on either the chromosome or large virulence plasmid of strain O157:H7. The pathogenicity island, LEE, and toxin-producing phage are encoded on the chromosome. The large virulence plasmid encodes multiple virulence factors including a hemolysin and clostridial-like toxins. All the latter horizontally acquired virulence genes encode traits that result in the damage of the host gut epithelium.

Citation: Mahenthiralingam E. 2004. Gene Associations in Bacterial Pathogenesis: Pathogenicity Islands and Genomic Deletions, p 249-274. In Miller R, Day M (ed), Microbial Evolution. ASM Press, Washington, DC. doi: 10.1128/9781555817749.ch16
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of FIGURE 7
FIGURE 7

The major mechanisms involved in the evolution of bacterial pathogen genomes. A bacterial genome is indicated by the black circle. Processes of additive evolution are indicated on the left, while the complementary mechanisms of reductive evolution are indicated on the right. Genes, gene clusters, and mobile genetic elements associated with evolution pathogenesis are shown as arrows or labeled features.

Citation: Mahenthiralingam E. 2004. Gene Associations in Bacterial Pathogenesis: Pathogenicity Islands and Genomic Deletions, p 249-274. In Miller R, Day M (ed), Microbial Evolution. ASM Press, Washington, DC. doi: 10.1128/9781555817749.ch16
Permissions and Reprints Request Permissions
Download as Powerpoint

References

/content/book/10.1128/9781555817749.chap16
1. Blattner, F. R.,, G. Plunkett III,, C. A. Bloch,, N. T. Perna,, V. Burland,, M. Riley,, J. Collado-Vides,, J. D. Glasner,, C. K. Rode,, G. F. Mayhew,, J. Gregor,, N. W. Davis,, H. A. Kirkpatrick,, M. A. Goeden,, D. J. Rose,, B. Mau,, and Y. Shao. 1997. The complete genome sequence of Escherichia coli K-12. Science 277:14531474.
2. Burland, V.,, Y. Shao,, N. T. Perna,, G. Plunkett,, H.J. Sofia,, and F. R. Blattner. 1998. The complete DNA sequence and analysis of the large virulence plasmid of Escherichia coli O157:H7. Nucleic Acids Res. 26:41964204.
3. Casadevall, A.,, and L. A. Pirofski. 2000. Host-pathogen interactions: basic concepts of microbial commensalism, colonization, infection, and disease. Infect. Immun. 68:65116518.
4. Cole, S. T.,, R. Brosch,, J. Parkhill,, T. Gamier,, C. Churcher,, D. Harris,, S. V. Gordon,, K. Eiglmeier,, S. Gas,, C. E. Barrylll,, F. Tekaia,, K. Badcock,, D. Basham,, D. Brown,, T. Chillingworth,, R. Connor,, R. Davies,, K. Devlin,, T. Feltwell,, S. Gentles,, N. Hamlin,, S. Holroyd,, T. Hornsby,, K. Jagels,, B. G. Barrell, et al. 1998. Deciphering the biology of Mycobacterium tuberculosis from the complete genome sequence. Nature. 393:537544.
5. Cole, S.T., , K. Eiglmeier,, J. Parkhill,, K. D. James,, N. R. Thomson,, P. R. Wheeler,, N. Honore,, T. Garnier,, C. Churcher,, D. Harris,, K. Mungall,, D. Basham,, D. Brown,, T. Chillingworth,, R. Connor,, R. M. Davies,, K. Devlin,, S. Duthoy,, T. Feltwell,, A. Fraser,, N. Hamlin,, S. Holroyd,, T. Hornsby,, K. Jagels,, C. Lacroix,, J. Maclean,, S. Moule,, L. Murphy,, K. Oliver,, M. A. Quail,, M. A. Rajandream,, K. M. Rutherford,, S. Rutter,, K. Seeger,, S. Simon,, M. Simmonds,, J. Skelton,, R. Squares,, S. Squares,, K. Stevens,, K. Taylor,, S. Whitehead,, J. R. Woodward,, and B. G. Barrell. 2001. Massive gene decay in the leprosy bacillus Nature.409:10071011.
6. Cornells, G. R.,, A. Boland,, A. P. Boyd,, C. Geuijen,, M. Iriarte,, C. Neyt,, M. P. Sory,, and I. Stainier. 1998. The virulence plasmid of Yersinia, an antihost genome. Microbiol. Mol. Biol. Rev. 62:13151352.
7. Cornells, G. R.,, and F. Van Gijsegem. 2000. Assembly and function of type III secretory systems. Annu. Rev. Microbiol. 54:735774.
8. Hacker, J.,, G. Blum-Oehler,, I. Muhldorfer,, and H. Tschape. 1997. Pathogenicity islands of virulent bacteria: structure, function and impact on microbial evolution. Mol. Microbiol. 23:10891097.
9. Maurelli, A. T.,, R. E. Fernandez,, C. A. Bloch,, C. K. Rode,, and A. Fasano. 1998. "Black holes" and bacterial pathogenicity: A large genomic deletion that enhances the virulence of Shigella spp. and enteroinvasive Escherichia coli. Proc. Natl. Acad. Sci. USA 95:39433948.
10. Mira, A.,, H. Ochman,, and N. A. Moran. 2001. Deletional bias and the evolution of bacterial genomes. Trends Genet. 17:589596.
11. Ochman, H.,, and I. B. Jones. 2000. Evolutionary dynamics of full genome content in Escherichia coli. EMBO J. 19:66376643.
12. Parkhill, J.,, G. Dougan,, K. D. James,, N. R. Thomson,, D. Pickard,, J. Wain,, C. Churcher,, K. L. Mungall,, S. D. Bentley,, M. T. Holden,, M. Sebaihia,, S. Baker,, D. Basham,, K. Brooks,, T. Chillingworth,, P. Connerton,, A. Cronin,, P. Davis,, R. M. Davies,, L. Dowd,, N. White,, J. Farrar,, T. Feltwell,, N. Hamlin,, A. Haque,, T. T. Hien,, S. Holroyd,, K. Jagels,, A. Krogh,, T. S. Larsen,, S. Leather,, S. Moule,, P. O'Gaora,, C. Parry,, M. Quail,, K. Rutherford,, M. Simmonds,, J. Skelton,, K. Stevens,, S. Whitehead,, and B. G. Barrell. 2001. Complete genome sequence of a multiple drug resistant Salmonella enterica serovar Typhi CT18. Nature. 413:848852.
13. Perna, N. T.,, G. Plunkett III,, V. Burland,, B. Mau,, J. D. Glasner,, D. J. Rose,, G. F. Mayhew,, P. S. Evans,, J. Gregor,, H. A. Kirkpatrick,, G. Posfai,, J. Hackett,, S. Klink,, A. Boutin,, Y. Shao,, L. Miller,, E.J. Grotbeck,, N. W. Davis,, A. Lim,, E. T. Dimalanta,, K. D. Potamousis,, J. Apodaca,, T. S. Anantharaman,, J. Lin,, G. Yen,, D. C. Schwartz,, R. A. Welch,, and F. R. Blattner. 2001. Genome sequence of enterohaemorrhagic Escherichia coli O157:H7. Nature. 409:529533.
14. Rajakumar, K.,, C. Sasakawa,, and B. Adler. 1997. Use of a novel approach, termed island probing, identifies the Shigella flexneri she pathogenicity island which encodes a homolog of the immunoglobulin A protease-like family of proteins. Infect. Immun. 65:46064614.
15. Rutherford, K.,, J. Parkhill,, J. Crook,, T. Horsnell,, P. Rice,, M. A. Rajandream,, and B. Barrell. 2000. Artemis: sequence visualization and annotation. Bioinformatics 16:944945.
16. Brogden, K.,, J. Roth,, T. Stanton,, C. Bolin,, F. C. Minion,, and M. J. Wannemuehler (ed.). 2000 Virulence Mechanisms of Bacterial Pathogens, 3rd ed. ASM Press, Washington, D.C.
17. Kaper, J. B.,, and J. Hacker (ed.). 1999. Pathogenicity Islands and Other Mobile Virulence Elements. ASM Press, Washington, D.C.
18. Salyers, A. A.,, and D. Dixie (ed). 2001. Bacterial Pathogenesis: A Molecular Approach, 2nd ed. ASM Press, Washington, D.C.
19. Winstanley, C.,, and C. A. Hart. 2001. Type III secretion systems and pathogenicity islands. J. Med. Microbiol. 50:116126.

Tables

Generic image for table
TABLE 1

Examples of classical pathogenicity islands and their features

Citation: Mahenthiralingam E. 2004. Gene Associations in Bacterial Pathogenesis: Pathogenicity Islands and Genomic Deletions, p 249-274. In Miller R, Day M (ed), Microbial Evolution. ASM Press, Washington, DC. doi: 10.1128/9781555817749.ch16
Generic image for table
TABLE 2

Defining features of serovar Typhi PAIs

Citation: Mahenthiralingam E. 2004. Gene Associations in Bacterial Pathogenesis: Pathogenicity Islands and Genomic Deletions, p 249-274. In Miller R, Day M (ed), Microbial Evolution. ASM Press, Washington, DC. doi: 10.1128/9781555817749.ch16

This is a required field
Please enter a valid email address
Please check the format of the address you have entered.
Approval was a Success
Invalid data
An Error Occurred
Approval was partially successful, following selected items could not be processed due to error