Background Bacterial genomes develop new mechanisms to tide them over the

Background Bacterial genomes develop new mechanisms to tide them over the imposing conditions they encounter during the course of their evolution. of some of the functionally characterised LGTs in each species has indicated that they may have a possible adaptive role. Conclusion The five Corynebacterial genomes sequenced to date have evolved by acquiring between 8 C 14% of their genomes L-779450 IC50 by LGT and some of these genes may have a role in adaptation. Background Bacterial genomes are constantly under pressure from the selective challenges of their surroundings. To overcome these hardships, bacterial genomes evolve via mechanisms in the form of genome modifications by gene loss [1-3], gene genesis by duplication, modifying existing genes by L-779450 IC50 mutations [4,5] or acquisition of new genes by lateral gene transfer (LGT) [6-13]. Recent studies indicate that LGT has a larger role in bacterial evolution than previously anticipated [14-19], accounting for anywhere between 1.6 C 32.6% of the genes in each individual genome [20]. Gene content varies dramatically even among strains belonging to a single bacterial species [21-23]; variations mostly resulting from gene loss [1-3] and/or acquisition of new genes by LGT [6-13]. LGT plays a significant role in the evolution of bacterial genomes and L-779450 IC50 provides them with a ready-to-use novel gene pool that helps them to adapt faster to their ever changing surroundings and foray into new ecological niches. Documented evidence shows that laterally acquired genes can transform an otherwise avirulent bacteria into a virulent form [24,25], protect pathogenic bacteria against antibiotics [26], increase the metabolic diversity of the recipient bacteria [12,27-29] or confer on it abilities to explore new challenging niches [30,31]. Keeping in mind the capability of LGTs to provide diverse adaptive features, we review some of the previous work done on lateral gene transfer in bacteria with an emphasis on the adaptive role PEPCK-C of these laterally acquired genes. We also provide evidence about the transient nature of most of the laterally acquired genes based on a maximum likelihood modeling of the gene insertions/deletions at various stages during the evolution of the Corynebacterium species. For the ease of discussion, we have classified the adaptive features into three major categories and will review each in turn: (1) Pathogenicity related features (2) Metabolic capabilities and (3) Survival under extreme environmental conditions. Pathogenicity related features There are many documented instances of the acquisition of virulence determinants in bacteria by the process of LGT [22,25,32-38], selected examples are discussed below. The acquisition of a 35 kb eaeA locus encoding proteins responsible for attaching and effacing lesions has transformed an avirulent Escherischia coli strain into an enteropathogenic strain [39], whereas the acquisition of pathogenicity islands (PAIs) ranging from 70C150 kb and encoding virulence realted proteins resulted in uropathogenic strains [40,41]. Lawrence and Ochman [7] have identified that about 18% of the genome of E.coli MG1655 was acquired by LGT and this laterally acquired DNA has “conferred properties permitting E.coli to explore otherwise unreachable ecological niches”. The genome of Salmonella enterica has two laterally acquired pathogenicity islands, SPI-1 and SPI-2 encoding proteins that help in apoptosis, entry into non-phagocytic cells and systemic infection [42], whereas Bacillus cereus genome has three laterally acquired genomic islands BCGI-1, BCGI-2 and BCGI-3 with genes encoding proteins responsible for antibiotic resistance, ferric anguibactin transport system and lantibiotic L-779450 IC50 biosynthesis leading to a better survival of B. cereus inside the host L-779450 IC50 [43]. The highly pathogenic strains of Yersinia pestis have a 102 kb High Pathogenicity Island (HPI) that contains the hms locus encoding the capacity to store hemin, yersinibactin-pesticin receptor and an iron-regulated high molecular weight protein enabling an increased level of pathogenicity and survival in their hosts [44]. The case with the cag pathogenicity island in Helicobacter pylori is similar. This laterally acquired region encodes many antigenic determinants and virulence factors indicating its role in pathogenesis [45]. A comparison of the virulent and benign strains of Dichelobacter nodosus, a principal causative agent of the ovine footrot, revealed that the acquisition of vap and.