Subsystem: Staphylococcal pathogenicity islands SaPI

This subsystem's description is:

Remarkably, nearly all bacterial toxins associated with specific clinical conditions (toxinoses) are encoded by mobile genetic elements. Examples are the toxins responsible for diphtheria, anthrax, tetanus, botulism, cholera, toxic shock, scarlet fever, exfoliative dermatitis, food poisoning, travelers diarrhea, shigella dysentery, necrotizing pneumonia, and others. An interesting example of this phenomenon is the family of related staphylococcal pathogenicity islands (SaPI) encoding superantigens (SAgs). These are 15–20 kb elements that occupy constant positions in the chromosomes of toxigenic strains, and are characterized by certain phage-related features, namely genes encoding integrases, helicases, and terminases, and the presence of flanking direct repeats (Novick, 2003). The majority carry endotoxin genes, but some seem to harbor other genes potentially conferring selective advantage, e.g. SaGIm encodes a homolog of a ferrichrome-binding subunit (FhuD) of an ABC transporter (Kuroda et al., 2001). The prototype element for the entire group, SaPI1 of Staphylococcus aureus RN4282, located near tyrB, encodes Toxic shock syndrome toxin (TSST-1) plus two other SAgs, SEK and SEL (Ruzin et al., 2001). Some members of the family are capable of specific interactions with certain phages leading to excision, amplification, and encapsidation. Notably, some copies are located in the proximity of prophages.

With these elements being very variable, we relied mostly on their specific integration sites (att) in the S. aureus genome for classification (see Table 1 - access via green "Illustrations" tab on top of this page). For the published elements we tried to keep the names suggested in the original publication, for all others - names were projected in accordance with their att sites.
Note, that if you view Subsystem spreadsheet with “show clusters” activated, the clustering of the first gene of each element (Integrase, columns 6,7) with one of the possible integration sites (columns 1-5) will reveal the element type. There can be more than one element present per genome. Also, in several strains only a degenerated integrase gene is be present at the att site (a scar from previous integration events??)

For more information, please check out the description and the additional notes tabs, below

DiagramFunctional RolesSubsystem SpreadsheetDescriptionAdditional Notes 
Group Alias
Abbrev.Functional RoleReactionsScenario ReactionsGOLiterature
SubsetsColoring
collapsed
expanded


  
Taxonomy Pattern 
Organism 
Domain
Variant [?] 
active
CICro*integraseFhuD*att_sitesMW0753MW0754SAR0365SAR0369SAR0371SAR0372SAR0385SAV0786SAV0787SAV0788SAV0789SAV0790SAV0791SAV0792SAV0793SAV0794SAV0795SAV0796SAV0797SAV0798SAV0799SAV0801SAV0808SAV2026SAV2027SAR0375MW0751SAV0800EarSEBSEKSELTSST
Remarkably, nearly all bacterial toxins associated with specific clinical conditions (toxinoses) are encoded by mobile genetic elements. Examples are the toxins responsible for diphtheria, anthrax, tetanus, botulism, cholera, toxic shock, scarlet fever, exfoliative dermatitis, food poisoning, travelers diarrhea, shigella dysentery, necrotizing pneumonia, and others. An interesting example of this phenomenon is the family of related staphylococcal pathogenicity islands (SaPI) encoding superantigens (SAgs). These are 15–20 kb elements that occupy constant positions in the chromosomes of toxigenic strains, and are characterized by certain phage-related features, namely genes encoding integrases, helicases, and terminases, and the presence of flanking direct repeats (Novick, 2003). The majority carry endotoxin genes, but some seem to harbor other genes potentially conferring selective advantage, e.g. SaGIm encodes a homolog of a ferrichrome-binding subunit (FhuD) of an ABC transporter (Kuroda et al., 2001). The prototype element for the entire group, SaPI1 of Staphylococcus aureus RN4282, located near tyrB, encodes Toxic shock syndrome toxin (TSST-1) plus two other SAgs, SEK and SEL (Ruzin et al., 2001). Some members of the family are capable of specific interactions with certain phages leading to excision, amplification, and encapsidation. Notably, some copies are located in the proximity of prophages.

With these elements being very variable, we relied mostly on their specific integration sites (att) in the S. aureus genome for classification (see Table 1 - access via green "Illustrations" tab on top of this page). For the published elements we tried to keep the names suggested in the original publication, for all others - names were projected in accordance with their att sites.
Note, that if you view Subsystem spreadsheet with “show clusters” activated, the clustering of the first gene of each element (Integrase, columns 6,7) with one of the possible integration sites (columns 1-5) will reveal the element type. There can be more than one element present per genome. Also, in several strains only a degenerated integrase gene is be present at the att site (a scar from previous integration events??)
References

1. Fitzgerald, J.R., Monday, S.R., Foster, T.J., Bohach, G.A., Hartigan, P.J., Meaney, W.J., Smyth, C.J., 2001. Characterization of a putative pathogenicity island from bovine Staphylococcus aureus encoding multiple superantigens. J. Bacteriol. 183, 63–70.

2. Holden MT, Feil EJ, Lindsay JA, et al., and Parkhill J. 2004. Complete genomes of two clinical Staphylococcus aureus strains: evidence for the rapid evolution of virulence and drug resistance. Proc Natl Acad Sci U S A. 101(26):9786-91.

3. Kuroda M, Ohta T, Uchiyama I, et al., Ogasawara N, Hayashi H, Hiramatsu K. 2001. Whole genome sequencing of meticillin-resistant Staphylococcus aureus. Lancet, 357(9264):1225-40.

4. Novick RP. 2003. Mobile genetic elements and bacterial toxinoses: the superantigen-encoding pathogenicity islands of Staphylococcus aureus. Plasmid 49(2):93-105.

5. Ruzin, A., Lindsay, J., Novick, R.P., 2001. Molecular genetics of SaPI1—a mobile pathogenicity island in Staphylococcus aureus. Mol. Microbiol. 41, 365–377.

6. Yarwood J.M., J.K. McCormick, M. L. Paustian, P.M. Orwin, V. Kapur, and P. M. Schlievert. 2002. Characterization and expression analysis of Staphylococcus aureus pathogenicity island 3. Implications for the evolution of staphylococcal pathogenicity islands. J. Biol. Chem. 277(15):13138-13147