Survival of the not-so-fit
© BioMed Central Ltd 2003
Published: 14 August 2003
Bordetella pertussis, B. parapertussis, and B. bronchiseptica are three related pathogens that cause whooping cough and other respiratory diseases in humans and animals. One hypothesis to explain the relationship among the disease agents is that acquisition of genes leads to a gain of function that confers specificity of host and symptoms on a particular species. In the August 10 Nature Genetics, Julian Parkhill and colleagues, based at the Sanger Institute, show by sequencing and comparison of the genomes of all three pathogens that it is a loss of genes and regulatory elements that has caused relatively recent independent derivations of B. pertussis and B. parapertussis from B. bronchiseptica, following rearrangements and insertions by insertion sequence elements (ISEs) in their genomes (Nature Genetics 2003, DOI:10.1038/Ng1227).
Parkhill et al. demonstrated this in part by the presence of unique gene sequences in B. bronchiseptica, the absence of evidence of horizontal gene transfer in B. bronchiseptica, and the presence of ISEs on the boundaries of rearrangements. From linear genomic comparison, they discovered that while B. parapertussis and B. bronchiseptica show a large degree of colinearity of genome organization, an unprecedented overall genomic rearrangement has occurred in B. pertussis, with short blocks of almost perfect conservation being broken up by nearly 150 individual rearrangements, 88% of which are bounded by ISEs. The authors also showed that both B. pertussis and B. parapertussis exhibit substantial gene loss and inactivation through pseudogene formation and that these genes function predominantly in transport, small-molecule metabolism, regulation, and surface structures.
"Such ISE expansions have previously been seen in rarely recombining organisms whose effective population size was greatly reduced by an evolutionary bottleneck... It may be that B. pertussis followed [its] evolutionary path owing to the opportunities for increased transmission rate provided by the increase in size and density of the populations of its specific host, Homo sapiens," conclude the authors.