Evolution of Pan-Genomes of Escherichia coli, Shigella spp., and Salmonella enterica

Abstract

cMultiple sequencing of genomes belonging to a bacterial species allows one to analyze and compare statistics and dynamics of the gene complements of species, their pan-genomes. Here, we analyzed multiple genomes of Escherichia coli, Shigella spp., and Salmonella enterica. We demonstrate that the distribution of the number of genomes harboring a gene is well approximated by a sum of two power functions, describing frequent genes (present in many strains) and rare genes (present in few strains). The virtual absence of Shigella-specific genes not present in E. coli genomes confirms previous observations that Shigella is not an independent genus. While the pan-genome size is increasing with each new strain, the number of genes present in a fixed fraction of strains stabilizes quickly. For instance, slightly fewer than 4,000 genes are present in at least half of any group of E. coli genomes. Comparison of S. enterica and E. coli pan-genomes revealed the existence of a common periphery, that is, genes present in some but not all strains of both species. Analysis of phylogenetic trees demonstrates that rare genes from the periphery likely evolve under horizontal transfer, whereas frequent periphery genes may have been inherited from the periphery genome of the common ancestor.

Defining the Phylogenomics of Shigella Species: a Pathway to Diagnostics

“…To identify genes differentially distributed between the E. coli and Shigella genomes, a large-scale BSR (LS-BSR) analysis was performed on 69 E. coli and 69 Shigella genomes (45). The results demonstrate that several genes, primarily associated with metabolism, are conserved in E. coli isolates and largely absent (n Ͻ 2) in Shigella isolates (Table 2); this stands in contrast to a recent study which suggested that no genes could be used to distinguish the two groups (47). In fact, some of the genes identified as being differentially present in E. coli and not in Shigella have been previously identified as being pathoadaptive for Shigella (48), suggesting that the analysis is valid.…”

Subspecies in the global human gut microbiome

“…To be able to determine population structure without relying on limited or biased sets of pan‐genomes (Gordienko et al , 2013), we explored the natural genomic variation of the human gut microbiome (Schloissnig et al , 2013; Luo et al , 2015; Nayfach et al , 2016; Lloyd‐Price et al , 2017; Truong et al , 2017). To this end, we assessed the microbial genetic landscape of 2,144 deeply sequenced human stool metagenomes from nine countries, spanning three continents, including published (Huttenhower et al , 2012; Qin et al , 2012; Karlsson et al , 2013; Le Chatelier et al , 2013; Zeller et al , 2014) as well as 298 newly generated ones (Table EV1).…”

“…(Johnson et al , 2006), for which specific subspecies are specialized for different environmental conditions (Biller et al , 2014). In regard to the human microbiome, extensive work has been undertaken to characterize population structure and describe subspecies in species that include pathogenic bacteria, such as Escherichia coli , different Salmonella species, and a few others, for which multiple typing schemes exist (Gordienko et al , 2013; Chakraborty et al , 2015; Bale et al , 2016; Sharma et al , 2016), but not for the vast majority of human gut commensals.…”

Comparative genome-scale modelling of Staphylococcus aureus strains identifies strain-specific metabolic capabilities linked to pathogenicity

“…The unique genome is heavily enriched in genes related to mobile elements (62%), with the other categories being poorly represented. This high proportion of mobile elements in the unique genome is similar to other organisms, including E. coli, and indicates that horizontal gene transfer (HGT) has had a large effect on S. aureus evolution (25)(26)(27). Indeed, the archaic MRSA clone, thought to be the ancestor strain of MRSA in Europe, obtained its methicillin resistance because of the horizontal transfer of the mecA gene from an unknown source (1).…”