The accessory genome of Pseudomonas aeruginosa

Abstract

Pseudomonas aeruginosa strains exhibit significant variability in pathogenicity and ecological flexibility. Such interstrain differences reflect the dynamic nature of the P. aeruginosa genome, which is composed of a relatively invariable "core genome" and a highly variable "accessory genome." Here we review the major classes of genetic elements comprising the P. aeruginosa accessory genome and highlight emerging themes in the acquisition and functional importance of these elements. Although the precise phenotypes endowed by the majority of the P. aeruginosa accessory genome have yet to be determined, rapid progress is being made, and a clearer understanding of the role of the P. aeruginosa accessory genome in ecology and infection is emerging.

FIG. 1.

ICEs are self-transmissible genomic islands that can transiently exist as circular extrachromosomal elements, are transferred by self-mediated conjugation, and undergo integrase-mediated chromosomal integration.

FIG. 2.

PAGI-5, PAPI-1, and pKLC102 share a similar modular structure. Gray lines indicate regions of similar sequence. Purple boxes represent putative integration (I), transfer (T), and maintenance (M) gene modules common to all three ICEs. The integration module consists of the xerC integrase gene. The maintenance modules include the genes encoding the ParE maintenance toxin and the Soj partitioning protein. The transfer modules include genes encoding a coupling protein and a conjugative relaxase as well as GI-type T4SS genes. A few select cargo regions unique to particular ICEs and shown to contribute to pathogenicity (P) are shown in dark green. A set of PAGI-5 cargo ORFs with a potential ecological (E) role in conferring mercury resistance are shown in light green. (Adapted from reference with permission.)

FIG. 3.

Elements of the P. aeruginosa accessory genome are associated with increased virulence in P. aeruginosa clinical isolates. The genomes of 35 P. aeruginosa isolates cultured from the airways of patients with ventilator-associated pneumonia were examined for the presence of three components of the accessory genome: exoU, NR-I, and NR-II. The laboratory strain PAO1 was included as a control. The exoU gene is part of PAPI-2, and NR-I and NR-II are cargo regions carried by PAGI-5. Virulence was quantified by measuring the LD₅₀ in a mouse model of acute pneumonia. The y axis has been inverted such that higher bars represent increased levels of virulence. All three genetic elements are found more commonly in highly pathogenic strains. (Adapted from reference with permission. Copyright 2003 Infectious Diseases Society of America.)

FIG. 4.

General structures of transposable elements and integrons. (A) Organization of a typical IS. Terminal inverted repeats are represented by gray bars labeled IRL (left inverted repeat) and IRR (right inverted repeat). A single open reading frame encoding the transposase tnp is between the inverted repeats. The transposase promoter (P) is partially contained within the IRL. (B) Organization of a composite transposon. One or more genes (light gray boxes labeled orf) are flanked by two usually identical insertion sequences (IS). Transposition is mediated by the IS-contained transposase recognizing the IRL of the first IS and the IRR of the second IS. (C) Organization of a Tn3-like complex transposon. Transposase and recombinase genes are represented by white boxes labeled tnpA and tnpR, respectively. Non-transposition-related coding sequences are represented by light gray boxes labeled orf. These coding sequences are frequently found in the context of integrons. (D) Organization of a typical class 1 integron. The 5′ conserved region consists of the integrase gene intI1 followed by the attI recombination site, represented by a small black box. A forward-directed promoter (P_c) within intI1 drives expression of gene cassettes. Gene cassettes (labeled orf1, orf2, and orf3) are separated by their attC sites (orange boxes). The 3′ conserved segment in most class 1 integrons consists of a truncated quaternary ammonium compound resistance gene (qacEΔ) fused with a sul1 sulfonamide resistance gene.