PinR mediates the generation of reversible population diversity in Streptococcus zooepidemicus
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Opportunistic pathogens must adapt to and survive in a wide range of complex ecosystems. Streptococcus zooepidemicus is an opportunistic pathogen of horses and many other animals, including man. The assembly of different surface architecture phenotypes from one genotype is likely to be crucial to the successful exploitation of such an opportunistic lifestyle. Construction of a series of mutants revealed that a serine recombinase, PinR, inverts 114 bp of the promoter of SZO_08560, which is bordered by GTAGACTTTA and TAAAGTCTAC inverted repeats. Inversion acts as a switch, controlling the transcription of this sortase-processed protein, which may enhance the attachment of S. zooepidemicus to equine trachea. The genome of a recently sequenced strain of S. zooepidemicus, strain 2329 (Sz2329), was found to contain a disruptive internal inversion of 7 kb of the FimIV pilus locus, which is bordered by TAGAAA and TTTCTA inverted repeats. This strain lacks pinR and we hypothesized that this inversion may have become irreversible following the loss of this recombinase. Active inversion of FimIV was detected in three strains of S. zooepidemicus: 1770 (Sz1770), B260863 (SzB260863) and H050840501 (SzH050840501), all of which encoded pinR. A deletion mutant of Sz1770 that lacked pinR was no longer capable of inverting its internal region of FimIV. Our data highlight redundancy in the PinR sequence recognition motif around a short TAGA consensus and suggest that PinR can reversibly influence the wider surface architecture of S. zooepidemicus, providing this organism with a bet-hedging solution to survival in fluctuating environments.
Steward , K F , Harrison , T , Robinson , C , Slater , J , Maskell , D J , Harris , S R , Holden , M T G & Waller , A S 2015 , ' PinR mediates the generation of reversible population diversity in Streptococcus zooepidemicus ' Microbiology , vol 161 , no. 5 , pp. 1105-1112 . DOI: 10.1099/mic.0.000057
Copyright 2015 The Authors. This is not the version of record of this article. This is an author accepted manuscript (AAM) that has been accepted for publication in Microbiology that has not been copy-edited, typeset or proofed. The Society for General Microbiology (SGM) does not permit the posting of AAMs for commercial use or systematic distribution. SGM disclaims any responsibility or liability for errors or omissions in this version of the manuscript or in any version derived from it by any other parties. The final version is available at 10.1099/mic.0.000057 2015.
This project was funded by a project grant from the Horserace Betting Levy Board (vet/prj/751).
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