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. 2008 Jul 16;3(7):e2683.
doi: 10.1371/journal.pone.0002683.

Evolution of Streptococcus pneumoniae and its close commensal relatives

Mogens Kilian  1 , Knud Poulsen, Trinelise Blomqvist, Leiv S Håvarstein, Malene Bek-Thomsen, Hervé Tettelin, Uffe B S Sørensen
Affiliations

Evolution of Streptococcus pneumoniae and its close commensal relatives

Mogens Kilian et al. PLoS One. .

Abstract

Streptococcus pneumoniae is a member of the Mitis group of streptococci which, according to 16S rRNA-sequence based phylogenetic reconstruction, includes 12 species. While other species of this group are considered prototypes of commensal bacteria, S. pneumoniae is among the most frequent microbial killers worldwide. Population genetic analysis of 118 strains, supported by demonstration of a distinct cell wall carbohydrate structure and competence pheromone sequence signature, shows that S. pneumoniae is one of several hundred evolutionary lineages forming a cluster separate from Streptococcus oralis and Streptococcus infantis. The remaining lineages of this distinct cluster are commensals previously collectively referred to as Streptococcus mitis and each represent separate species by traditional taxonomic standard. Virulence genes including the operon for capsule polysaccharide synthesis and genes encoding IgA1 protease, pneumolysin, and autolysin were randomly distributed among S VSports手机版. mitis lineages. Estimates of the evolutionary age of the lineages, the identical location of remnants of virulence genes in the genomes of commensal strains, the pattern of genome reductions, and the proportion of unique genes and their origin support the model that the entire cluster of S. pneumoniae, S. pseudopneumoniae, and S. mitis lineages evolved from pneumococcus-like bacteria presumably pathogenic to the common immediate ancestor of hominoids. During their adaptation to a commensal life style, most of the lineages gradually lost the majority of genes determining virulence and became genetically distinct due to sexual isolation in their respective hosts. .

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Conflict of interest statement

Competing Interests: The authors have declared that no competing interests exist.

Figures

Figure 1
Figure 1. Phylogenetic tree constructed with the minimum evolution algorithm in MEGA version 4.0 and based on concatenated partial sequences of the house-keeping enzyme genes ddl, gdh, rpoB, and sodA.
Type strains of individual species are shown with species designation. Bootstrap values (%) are based on 1000 replications. The three major clusters supported by significant bootstrap values are the pneumoniae-mitis-pseudopneumoniae cluster (red lines), the Oralis cluster (blue lines), and the Infantis cluster (green lines). The subcluster of S. pneumoniae strains within the pneumoniae-mitis-pseudopneumoniae cluster is indicated by dark red lines (ruby), S. pseudoneumoniae strains within the pneumoniae-mitis-pseudopneumoniae cluster are indicated by pink, and strains previously assigned to “S. mitis biovar 2” within the Oralis cluster are indicated by dark blue lines. The random presence of homologues of virulence factors usually associated with S. pneumoniae (cap locus, capsule synthesis operon; iga, IgA1 protease gene; lytA, autolysin gene; ply, pneumolysin gene) in the diverse population of Mitis lineages is illustrated. A red signature indicates presence of the virulence gene, and black signature indicates a PCR product size compatible with absence of the gene. Black squares with a red center indicate IgA1 protease activity but an amplicon size in support of lack of an iga gene in the context found in S. pneumoniae. No signature indicates lack of a PCR product presumably due to no match of the primers. The arrow indicates the hypothetical immediate common ancestor of the red cluster. The scale bar refers to genetic divergence as calculated by the MEGA software.
Figure 2
Figure 2. Examples of long range PCR for detection of virulence genes.
Lane 1, molecular weight marker (sizes in kb are shown to the left); lanes 2–6, S. pneumoniae strains TIGR4, SK848, SK851, SK856, and SK858; lanes 7 and 8, S. pseudopneumoniae strains SK1069 and SK674; lanes 9–12, S. mitis strains SK575, SK568, SK142, and T2186; lanes 13 and 14, S. oralis strains SK23 and SK141. (A) PCR with primers aliA and dexB flanking the cap gene cluster. Amplicons larger than 7 kb represent the area between the genes aliA and dexB, whereas partial sequencing and control PCRs revealed that the smaller ones in lanes 7–13 are artifacts due to amplification of different regions with the aliA primer alone. The S. pseudopneumoniae, S. mitis, and S. oralis strains were selected to illustrate these artifacts. (B) and (C) Amplicons resulting from PCR with primers flanking the ply-lytA region and the iga gene, respectively.
Figure 3
Figure 3. Map of S. pneumoniae genomes –, and the unfinished S. mitis genome (JCVI CMR) in the area that includes the IgA1 protease gene (iga).
The map shows synteny apart from the absent iga gene in S. mitis NCTC 12261, in agreement with its lack of IgA1 protease activity, and apart from an additional iga paralog (zmpD) in some pneumococcus strains (INV200 and 23F) and in two strains of S. mitis .
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