Published online 7 November 2005
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Genome dynamics and diversity of Shigella species, the etiologic agents of bacillary dysentery
1State Key Laboratory for Molecular Virology and Genetic Engineering, Chinese Ministry of Public Health Beijing 100052, China 2Microbial Genome Research Center, Chinese Ministry of Public Health Beijing 100052, China 3National Center of Human Genome Research Beijing 100176, China 4The Wellcome Trust Sanger Institute Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SA, UK
*To whom correspondence should be addressed. Tel: +86 10 6787 7732; Fax: +86 10 6787 7736; Email: zdsys{at}sina.com
Received August 15, 2005. Revised September 21, 2005. Accepted October 19, 2005.
The Shigella bacteria cause bacillary dysentery, which remains a significant threat to public health. The genus status and species classification appear no longer valid, as compelling evidence indicates that Shigella, as well as enteroinvasive Escherichia coli, are derived from multiple origins of E.coli and form a single pathovar. Nevertheless, Shigella dysenteriae serotype 1 causes deadly epidemics but Shigella boydii is restricted to the Indian subcontinent, while Shigella flexneri and Shigella sonnei are prevalent in developing and developed countries respectively. To begin to explain these distinctive epidemiological and pathological features at the genome level, we have carried out comparative genomics on four representative strains. Each of the Shigella genomes includes a virulence plasmid that encodes conserved primary virulence determinants. The Shigella chromosomes share most of their genes with that of E.coli K12 strain MG1655, but each has over 200 pseudogenes, 300
700 copies of insertion sequence (IS) elements, and numerous deletions, insertions, translocations and inversions. There is extensive diversity of putative virulence genes, mostly acquired via bacteriophage-mediated lateral gene transfer. Hence, via convergent evolution involving gain and loss of functions, through bacteriophage-mediated gene acquisition, IS-mediated DNA rearrangements and formation of pseudogenes, the Shigella spp. became highly specific human pathogens with variable epidemiological and pathological features.
The authors wish it to be known that, in their opinion, the first four authors should be regarded as joint First Authors
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