Evolutionary biology of bacterial and fungal pathogens
Abstract
This chapter reviews emerging themes from genome sequence data and microarray whole genome comparisons of the pathogenic yersiniae and discusses how this information is guiding hypotheses on the evolution of Yersinia. The factors influencing the rise and fall of plague epidemics remain obscure, but it is possible that severe epidemics may be preceded by subtle genetic changes in Y. pestis resulting in a highly virulent strain. A large-scale comparison of the new Y. pestis and Y. pseudotuberculosis sequences should allow the comparative evolution of Y. pestis to be investigated in great detail and key acquisitions and mutations to be identified. A striking feature of the Y. pestis CO92 genome sequence is the large number of insertion sequence (IS) elements. A total of 140 IS elements comprises 3.7% of the genome. Recombination between two IS100 elements is likely to be responsible for the extreme in vitro instability of the hms locus in Y. pestis. Several genetic mechanisms account for the accumulation of pseudogenes in Y. pestis, including IS element expansion, deletion, point mutation, and slippage in tracts of single-nucleotide repeats. When pathogenic Shigella strains arose from a nonpathogenic Escherichia coli ancestor, the loss of ompT and cadA genes (so-called black holes) may have contributed to their virulence and evolution.
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