Pathogenicity Islands and Their Role in Staphylococcal Biology

Abstract

Pathogenicity islands are members of a vast collection of genomic islands that encode important virulence, antibiotic resistance and other accessory functions and have a critical role in bacterial gene transfer. Staphylococcus aureus is host to a large family of such islands, known as SaPIs, which encode super antigen and other virulence determinants, are mobilized by helper phages and transferred at extremely high frequencies. They benefit their host cells by interfering with phage predation and enhancing horizontal gene transfer. This chapter describes their life cycle, the bases of their phage interference mechanisms, their transfer system and their conversion to antibacterial agents for treatment ofstaphylococcal infections.

FIGURE 1

The SaPI genome and its putative origin. (A) Block diagrams. At the top is a typical prophage genome, and below that is the putative SaPI precursor, presumably the result of a major deletion. Next are two extant SaPI genomes. (B) Genetic maps of SaPI1 and SaPIbov5. Colors: red, interference genes; aqua, terS; orange, accessory genes; blue, regulatory genes; yellow, int/xis; gray, hypotheticals; purple, replication.

FIGURE 2

SaPI genomic pattern. At the top is the groEL region of S. aureus strain mu50, with a classical SaPI inserted at the 3′ end of groEL. The basic SaPI genes are in gray, and accessory genes at the left end are in green. Note the typical transcriptional divergence. Below is shown the corresponding region of strain JH9, in which the SaPI att site at groEL is empty.

FIGURE 3

The SaPI life cycle.

FIGURE 4

Induction, maturation, release, and cell killing by a CRISPR/cas9 ABD.

FIGURE 5

Diagrammatic representation of the ABD backbone.