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Category: Genomics and Bioinformatics; Bacterial Pathogenesis
Impact of Phages on Evolution of Bacterial Pathogenicity, Page 1 of 2
< Previous page | Next page > /docserver/preview/fulltext/10.1128/9781555815530/9781555814519_Chap11-1.gif /docserver/preview/fulltext/10.1128/9781555815530/9781555814519_Chap11-2.gifAbstract:
An interesting facet of Streptococcus pyogenes and Staphylococcus aureus, is their double role as commensals and pathogens. In this context, certain aspects of bacterial pathogenicity can be interpreted as a recall of antipredation strategies that bacteria evolved against phagocytosis by protozoan grazers. Many bacteria contain multiple genomes of bacterial viruses in their chromosomes. Prophage DNA can constitute a sizable part of the total bacterial DNA. When genomes from closely related bacteria were compared in a dot plot analysis, prophage sequences frequently accounted for a substantial, if not major, part of the differences between the genomes. Prophages can be present in many different forms, ranging from inducible prophages via prophages showing deletions, insertion, and rearrangements, to prophage remnants that lost most of the phage genome. In prophages from gram-negative bacteria, “extra” genes were identified near both prophage DNA ends. Prophages seem to be only transient passengers on the bacterial chromosomes, at least when seen on an evolutionary timescale. In an appealing model, the emergence of new, unusually virulent subclones of M3 strains is explained by the sequential acquisition of prophages, suggesting bacterial pathogenicity evolution in the fast lane. The virulence genes have certainly not evolved in phages but are the result of close bacterial interaction with the eukaryotic cell. Phages are perhaps only the handy gene carriers efficiently shuttling genes around in the bacterial world.
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Genome alignment of S. pyogenes serotype M18 (vertical) against serotype M3 (horizontal) shows that practically all diversity is prophage induced. Regions of nonalignment are circled, and prophages are marked with rectangles.
S. pyogenes prophage inactivation by point mutations in DNA replication or DNA assembly proteins (vertical black arrow). Virulence genes are circled.
Dot plot matrix of S. pyogenes prophages identified in S. pyogenes sequencing projects.
Selective list of virulence genes encoded on prophages.
Genome organization of a typical S. pyogenes prophage encoding two virulence factors (circled).