Bacterial contingency loci: the role of simple sequence DNA repeats in bacterial adaptation.
Bacterial pathogens face stringent challenges to their survival because of the many unpredictable, often precipitate, and dynamic changes that occur in the host environment or in the process of transmission from one host to another. Bacterial adaptation to their hosts involves either a mechanism for sensing and responding to external changes or the selection of variants that arise through mutation. Here we review how bacterial pathogens exploit localized hypermutation, through polymerase slippage of simple sequence repeats (SSRs), to generate phenotypic variation and enhanced fitness. These SSRs are located within the reading frame or in the promoter of a subset of genes, often termed contingency loci, whose functions are usually involved in direct interactions with host structures.
Moxon
Richard
R
Oxford University Department of Paediatrics, Molecular Infectious Diseases Group, Weatherall Institute of Molecular Medicine Oxford, United Kingdom. moxon@hammer.imm.ox.ac.uk
Bayliss
Chris
C
Hood
Derek
D
D000222:Adaptation, Physiological; D001483:Base Sequence; D004269:DNA, Bacterial / Q000737:chemistry* / Q000378:metabolism; D005798:Genes, Bacterial; D014644:Genetic Variation; D006193:Haemophilus influenzae / Q000235:genetics / Q000378:metabolism / Q000472:pathogenicity; D018895:Microsatellite Repeats; D008969:Molecular Sequence Data; D009154:Mutation; D016366:Open Reading Frames; D010641:Phenotype
D004269:DNA, Bacterial