A biphasic epigenetic switch controls immunoevasion, virulence and niche adaptation in non-typeable Haemophilus influenzae

John M. Atack, Yogitha N. Srikhanta, Kate L. Fox, Joseph A. Jurcisek, Kenneth L. Brockman, Tyson A. Clark, Matthew Boitano, Peter M. Power, Freda E.-C. Jen, Alastair G. McEwan, Sean M. Grimmond, Arnold L. Smith, Stephen J. Barenkamp, Jonas Korlach, Lauren O. Bakaletz () and Michael P. Jennings ()
Additional contact information
John M. Atack: Institute for Glycomics, Griffith University
Yogitha N. Srikhanta: Institute for Glycomics, Griffith University
Kate L. Fox: School of Chemistry and Molecular Biosciences, The University of Queensland, St Lucia
Joseph A. Jurcisek: Center for Microbial Pathogenesis, The Research Institute at Nationwide Children’s Hospital and The Ohio State University College of Medicine
Kenneth L. Brockman: Center for Microbial Pathogenesis, The Research Institute at Nationwide Children’s Hospital and The Ohio State University College of Medicine
Tyson A. Clark: Pacific Biosciences
Matthew Boitano: Pacific Biosciences
Peter M. Power: Institute for Glycomics, Griffith University
Freda E.-C. Jen: Institute for Glycomics, Griffith University
Alastair G. McEwan: School of Chemistry and Molecular Biosciences, The University of Queensland, St Lucia
Sean M. Grimmond: Institute of Molecular Bioscience, The University of Queensland, St Lucia
Arnold L. Smith: Center for Global Infectious Disease Research, Seattle Children's Research Institute
Stephen J. Barenkamp: Saint Louis University School of Medicine, and the Pediatric Research Institute, Cardinal Glennon Children’s Medical Center
Jonas Korlach: Pacific Biosciences
Lauren O. Bakaletz: Center for Microbial Pathogenesis, The Research Institute at Nationwide Children’s Hospital and The Ohio State University College of Medicine
Michael P. Jennings: Institute for Glycomics, Griffith University

Nature Communications, 2015, vol. 6, issue 1, 1-12

Abstract: Abstract Non-typeable Haemophilus influenzae contains an N6-adenine DNA-methyltransferase (ModA) that is subject to phase-variable expression (random ON/OFF switching). Five modA alleles, modA2, modA4, modA5, modA9 and modA10, account for over two-thirds of clinical otitis media isolates surveyed. Here, we use single molecule, real-time (SMRT) methylome analysis to identify the DNA-recognition motifs for all five of these modA alleles. Phase variation of these alleles regulates multiple proteins including vaccine candidates, and key virulence phenotypes such as antibiotic resistance (modA2, modA5, modA10), biofilm formation (modA2) and immunoevasion (modA4). Analyses of a modA2 strain in the chinchilla model of otitis media show a clear selection for ON switching of modA2 in the middle ear. Our results indicate that a biphasic epigenetic switch can control bacterial virulence, immunoevasion and niche adaptation in an animal model system.

Date: 2015
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DOI: 10.1038/ncomms8828

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