The transposon-like correia elements encode numerous strong promoters and provide a potential new mechanism for phase variation in the meningococcus

Neisseria meningitidis is the primary causative agent of bacterial meningitis. the genome is rich in repetitive dna and almost 2% is occupied by a diminutive transposon called the correia element. here we report a bioinformatic analysis defining eight subtypes of the element with four distinct types of ends. transcriptional analysis,using pcr and a lacz reporter system,revealed that two ends in particular encode strong promoters. the activity of the strongest promoter is dictated by a recurrent polymorphism (y128) at the right end of the element. we highlight examples of elements that appear to drive transcription of adjacent genes and others that may express small non-coding rnas. pair-wise comparisons between three meningococcal genomes revealed that no more than two-thirds of correia elements maintain their subtype at any particular locus. this is due to recombinational class switching between elements in a single strain. upon switching subtype,a new allele is available to spread through the population by natural transformation. this process may represent a hitherto unrecognized mechanism for phase variation in the meningococcus. we conclude that the strain-to-strain variability of the correia elements,and the large number of strong promoters encoded by them,allows for potentially widespread effects within the population as a whole. by defining the strength of the promoters encoded by the eight subtypes of correia ends,we provide a resource that allows the transcriptional effects of a particular subtype at a given locus to be predicted. © 2011 siddique et al.