Later, such large unstable chromosomal

find more regions were designated pathogenicity islands (PAIs) [2–4]. A constantly increasing number of similar genetic elements detected in many pathogenic and non-pathogenic microorganisms led to the definition of a family of related genetic elements, termed genomic islands (GEIs), whose members share characteristic features [5–7]. Although PAIs, a subgroup of GEIs, are in several cases superficially similar, they structurally differ with respect to the encoded virulence factors, the size and the presence of different mobile and ARN-509 accessory elements. Due to the presence of mobility genes (integrases, transposases, IS elements) or the occurrence of recombination processes or point mutations, PAIs constantly undergo structural changes [4, 8–12]. Upon acquisition and chromosomal insertion, islands together with additional large regions of flanking chromosomal sequence context can be transferred by conjugation and homologous recombination and thus contribute to genome plasticity and the simultaneous transfer of multiple traits [13]. Nevertheless, PAIs are in many cases not stably integrated into the E. coli host chromosome and may be lost upon deletion. This process can be studied by island probing [10, 14–16]. The influence of different environmental conditions on the stability www.selleckchem.com/products/lgk-974.html of five PAIs of UPEC strain 536 has already been investigated before

[17] indicating that PAI I536, PAI II536, PAI III536, and PAI V536 delete with frequencies between 10-5 and 10-6, while loss of PAI IV536 could not be detected. In UPEC strain 536, PAI deletion is catalyzed by a P4-like

bacteriophage integrase which is encoded on the respective island [18]. Similar deletion frequencies (10-5 – 10-6) were also reported for PAIs of REPEC strain 84/110-1 and S. flexneri 2a [12, 19]. Higher deletion frequencies (10-3 – 10-4) have, Adenosine however, been observed for O-islands 43 and 48 in enterohemorrhagic E. coli (EHEC) O157:H7 isolates [14]. Circular intermediate (CI) formation in the cytoplasm of UPEC strain 536 was demonstrated for PAI II536 and PAI III536. Since none of these two islands apparently contain an origin of replication, it has been hypothesized that CIs are lost upon cell division unless they reintegrate into the chromosome. Furthermore, horizontal gene transfer (HGT) of such circularized PAIs may occur with the help of bacteriophages or conjugative plasmids [17]. A close functional association between PAIs and bacteriophages was reported for several bacterial pathogens. In V. cholerae, the entire 39.5-kb Vibrio Pathogenicity Island (VPI) can be transfered by the general transducing phage CP-T1 [20]. The “”high pathogenicity island (HPI)”" of Yersinia pseudotuberculosis has been shown to be transfered by a bacteriophage [21]. The so-called Staphylococcus aureus pathogenicity islands (SaPIs) can excise and replicate upon induction by other resident S.