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

Siddique, Azeem; Buisine, Nicolas; Chalmers, Ronald

Abstract

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.

Citation

Siddique, A., Buisine, N., & Chalmers, R. (2011). The transposon-like correia elements encode numerous strong promoters and provide a potential new mechanism for phase variation in the meningococcus. PLoS Genetics, 7(1), Article 13. https://doi.org/10.1371/journal.pgen.1001277

• Journal Article Type: Article
• Publication Date: Jan 20, 2011
• Deposit Date: Apr 23, 2014
• Publicly Available Date: Apr 23, 2014
• Journal: PLoS Genetics
• Print ISSN: 1553-7390
• Electronic ISSN: 1553-7404
• Publisher: Public Library of Science
• Peer Reviewed: Peer Reviewed
• Volume: 7
• Issue: 1
• Article Number: 13
• DOI: https://doi.org/10.1371/journal.pgen.1001277
• Public URL: https://nottingham-repository.worktribe.com/output/707132
• Publisher URL: http://www.plosgenetics.org/article/info%3Adoi%2F10.1371%2Fjournal.pgen.1001277