Genome Plasticity in Salmonella enterica and Its Relevance to Host-Pathogen Interactions

Abstract

Genome plasticity in Salmonella was first detected in Salmonella enterica serovar Typhi. It has been observed in a number of Salmonella serovars since then. Mechanisms that can lead to alterations in the genome include changes at the single-nucleotide level, gene loss, and genome rearrangements. Genome rearrangements including inversions and translocations can lead to genome plasticity, contributing to the divergence of Salmonella strains. Salmonella pathogenicity islands (SPIs) are large regions of DNA, which are most likely acquired as a result of horizontal gene transfer (HGT) and are often associated with virulence. The virulence plasmids of Salmonella strains contribute to the adaptation of the organism, and in some cases allow the transfer of genes. It appears that expansion of host range is linked to lateral gene transfer (LGT) of genes involved in host-pathogen interactions. A common theme for the variable regions between serovars was the diversity in sugar metabolism, highlighting the redundancy of these systems. The majority of coding regions unique to serovar Enteritidis encode prophage-related functions. Although the genome sequence of S. enterica serovar Pullorum is found to be very similar to those of other Salmonella serovars, the genetic arrangement was significantly different, with three major inversions and one translocation found between strains. Understanding the phenomenon of genome plasticity in this species is important to characterize the relationship between genetic variation and host adaptation, as well as the ability to cause a relatively minor gastrointestinal disease or a potentially life-threatening systemic fever.