Pathogenicity island

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Pathogenicity islands (PAIs), as termed in 1990, are a distinct class of genomic islands acquired by microorganisms through horizontal gene transfer. [1] [2] Pathogenicity islands are found in both animal and plant pathogens. [2] Additionally, PAIs are found in both gram-positive and gram-negative bacteria. [2] They are transferred through horizontal gene transfer events such as transfer by a plasmid, phage, or conjugative transposon. [3] Therefore, PAIs enables microorganisms to induce disease and also contribute to microorganisms' ability to evolve.

Contents

Although the general makeup of pathogenicity islands (PAIs) might vary throughout bacterial pathogen strains, all PAIs are known to have characteristics with all genomic islands, including virulence genes, functional mobility elements, and areas of homology to tRNA genes and direct repeats. [2] [4]

One species of bacteria may have more than one PAI. For example, Salmonella has at least five. [5]

An analogous genomic structure in rhizobia is termed a symbiosis island .

Properties

Pathogenicity islands (PAIs) are gene clusters incorporated in the genome, chromosomally or extrachromosomally, of pathogenic organisms, but are usually absent from those nonpathogenic organisms of the same or closely related species. [2] [6] [7] They may be located on a bacterial chromosome or may be transferred within a plasmid or can be found in bacteriophage genomes. [2] The GC-content and codon usage of pathogenicity islands often differs from that of the rest of the genome, potentially aiding in their detection within a given DNA sequence, unless the donor and recipient of the PAI have similar GC-content. [2]

The most basic kind of mobile genetic element is an insertion sequence (IS), which usually just has one or two open reading frames that encode genes to make transposition easier. The majority are surrounded by brief terminal inverted repeats that serve as homologous recombination sites, enhancing a PAI's stability. [8] Sections inside the PAI can be rearranged or deleted with the use of IS components. [2] Such changes are probably going to encourage adaption and aid in the emergence of alternative strains. [8] PAIs are flanked by direct repeats; the sequence of bases at two ends of the inserted sequence are the same. Bacteriophage integrases, enzymes produced by bacteriophages that enable site-specific recombination between two recognition sequences, are another common mobility element found on pathogenicity islands (PAIs) to enable insertion into host DNA. [2] PAIs are often associated with tRNA genes, which target sites for this integration event. [2] They can be transferred as a single unit to new bacterial cells, thus conferring virulence to formerly benign strains. [6]

PAIs, a type of mobile genetic element, may range from 10-200 kb and encode genes which contribute to the virulence of the respective pathogen. [2] Pathogenicity islands carry genes encoding one or more virulence factors, including, but not limited to, adhesins, secretion systems (like type III secretion system), toxins, invasins, modulins, effectors, superantigens, iron uptake systems, o-antigen synthesis, serum resistance, immunoglobulin A proteases, apoptosis, capsule synthesis, and plant tumorigenesis via Agrobacterium tumefaciens . [2]

There are various combinations of regulation involving pathogenicity islands. The first combination is that the pathogenicity island contains the genes to regulate the virulence genes encoded on the PAI. [2] The second combination is that the pathogenicity island contains the genes to regulate genes located outside of the pathogenecity island. [2] Additionally, regulatory genes outside of the PAI may regulate virulence genes in the pathogenicity island. [2] Regulation genes typically encoded on PAIs include AraC-like proteins and two-component response regulators. [2]

PAIs can be considered unstable DNA regions as they are susceptible to deletions or mobilization. [2] This may be due to the structure of PAIs, with direct repeats, insertion sequences and association with tRNA that enables deletion and mobilization at higher frequencies. [3] Additionally, deletions of pathogenicity islands inserted in the genome can result in disrupting tRNA and subsequently affect the metabolism of the cell. [6]

Examples

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References

  1. ↑ Hacker, J; Bender, L; Ott, M; et al. (1990). "Deletions of chro- mosomal regions coding for fimbriae and hemolysins occur in vivo and in vitro in various extraintestinal Escherichia coli iso- lates". Microb. Pathog. 8 (3): 213–25. doi:10.1016/0882-4010(90)90048-U. PMID   1974320.
  2. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 Hacker, J; Kaper, JB (2000). "Pathogenicity Islands and the Evolution of Microbes". Annual Review of Microbiology. 54: 641–679. doi:10.1146/annurev.micro.54.1.641. ISSN   0066-4227. PMID   11018140. S2CID   1945976.
  3. 1 2 3 4 Hacker, J.; Blum-Oehler, G.; Muhldorfer, I.; Tschape, H. (1997). "Pathogenecity islands of virulent bacteria: structure, function and impact on microbial evolution". Molecular Microbiology. 23 (6): 1089–1097. doi: 10.1046/j.1365-2958.1997.3101672.x . PMID   9106201. S2CID   27524815.
  4. ↑ Gal-Mor, Ohad; Finlay, B. Brett (2006). "Pathogenicity islands: a molecular toolbox for bacterial virulence". Cellular Microbiology. 8 (11): 1707–1719. doi: 10.1111/j.1462-5822.2006.00794.x . ISSN   1462-5822. PMID   16939533.
  5. ↑ Marcus, Sandra L.; Brumell, John H.; Pfeifer, Cheryl G.; Finlay, B. Brett (2000-02-01). "Salmonella pathogenicity islands: big virulence in small packages". Microbes and Infection. 2 (2): 145–156. doi:10.1016/S1286-4579(00)00273-2. ISSN   1286-4579.
  6. 1 2 3 4 Groisman E (1996). "Pathogenicity Islands: Bacterial Evolution in Quantum Leaps". Cell. 87 (5): 791–794. doi: 10.1016/s0092-8674(00)81985-6 . PMID   8945505. S2CID   173554.
  7. ↑ Kaper JB, Hacker J, eds. 1999. Pathogenicity Islands and Other Mobile Virulence Elements. Washington, DC: Am. Soc. Microbiol. 1-11.
  8. 1 2 Hallstrom, Kelly N.; McCormick, Beth A. (2015). "Pathogenicity Islands: Origins, Structure, and Roles in Bacterial Pathogenesis". Molecular Medical Microbiology. Academic Press. pp. 303–314. doi:10.1016/b978-0-12-397169-2.00016-0. ISBN   978-0-12-397169-2.
  9. ↑ Nakano M. et al. 2001 Structural and sequence diversity of the pathogenicity island of uropathogenic Escherichia coli which encodes the USP protein
  10. ↑ Lindsay, JA; Ruzin, A; Ross, HF; et al. (Jul 1998). "The gene for toxic shock toxin is carried by a family of mobile pathogenicity islands in Staphylococcus aureus". Molecular Microbiology. 29 (2): 527–43. doi: 10.1046/j.1365-2958.1998.00947.x . PMID   9720870. S2CID   30680160.
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