Dr Christopher D.Bayliss
RCUK Research Fellow
Tel: +44 (0)116 252 3465
Fax: +44 (0)116 252 3378
I grew up in rural villages of Surrey and South Yorkshire. In 1997, I joined a team at the Weatherall Institute for Molecular Medicine, Oxford, dedicated to investigating the mechanisms responsible for surface variability in two bacterial pathogens responsible for meningitis.
After completing my first degree in Microbiology (Aberystwyth, University College of Wales), I went on to clone and sequence a dsRNA virus of chickens as part of my PhD at Houghton Poultry Research Institute in Cambridgeshire. I then undertook two three-year research projects on the molecular biology of vaccinia virus, firstly in the University of Florida, located in Gainesville, and then back across the Atlantic in Oxford. I also held a Welcome Trust Value in People Award at the University of Nottingham, and obtained an RCUK Research Fellow in the Department of Genetics, University of Leicester in 2007 lead an active research group with an interest in hypermutable DNA sequences.
I also held a Welcome Trust Value in People Award at the University of Nottingham, and obtained an RCUK Research Fellow in the Department of Genetics, University of Leicester in 2007 lead an active research group with an interest in hypermutable DNA sequences.
MSc in Molecular Medical Genetics: Project Supervisor
BS3009 Genomics: A Microbial Perspective:Co-convenor
BS3012 Infection and Immunity
Genetic Modification Sub-Committee member
Outreach: talks to Meningitis Research Foundation
C.D. Bayliss, J.C. Hoe, K. Makepeace, P. Martin, D.W. Hood and E.R. Moxon (2008). Escape by Neisseria meningitidis of the Bactericidal Activity of a Monoclonal Antibody is Mediated by Phase Variation of lgtG and Enhanced by a Mutator Phenotype. Infect. Immun. 76: 5038-5048.
C.D. Bayliss (2009). Determinants of phase variation rate and the fitness implications of differing rates for bacterial pathogens. FEMS Microbiol. Rev. 33: 504-520.
C.D. Bayliss , J.C. Hoe, K. Makepeace, P. Martin, D.W. Hood and E.R. Moxon (2008). Neisseria meningitidis escape from the bactericidal activity of a monoclonal antibody is mediated by phase variation of lgtG and enhanced by a mutator phenotype. Infection and Immunity 76:5038-48.
K.M. Dixon, C.D. Bayliss, K. Makepeace, E.R. Moxon and D.W. Hood (2007). Identification of the Functional Initiation Codons of a Phase Variable Gene of Haemophilus influenzae, lic2A, with the Potential for Differential Expression. Journal of Bacteriology 189: 511-521.
C.D. Bayliss, M.J. Callaghan and E.R. Moxon (2006). High allelic diversity in the methyltransferase gene of a phase variable type III restriction-modification system has implications for the fitness of Haemophilus influenzae. Nucleic Acids Research 34: 4046-4059.
C.D. Bayliss, W.A. Sweetman and E.R. Moxon (2005). Tetranucleotide repeats are destabilised in Haemophilus influenzae mutants lacking RnaseHI and the Klenow domain of PolI. Nucleic Acids Research 33: 400-408.
W.A. Sweetman, E.R. Moxon and C.D. Bayliss (2005). Induction of the SOS regulon of Haemophilus influenzae does not effect phase variation rates at tetranucleotide or dinucleotide repeats. Microbiology 151: 2751-2763.
R. Griffin, C.D. Bayliss, M. Herbert, C. Makepeace, D.W. Hood and E.R. Moxon (2005). Digalactoside expression in the lipopolysaccharide of Haemophilus influenzae: role in intravascular survival. Infection and Immunity 73, 7022-7026.
C.D. Bayliss, W.A. Sweetman and E.R. Moxon (2004). Mutations in Haemophilus influenzae Mismatch Repair Genes Increase Mutation Rates of Dinucleotide Repeat Tracts but Not Dinucleotide Repeat-Driven Pilin Phase Variation Rates. Journal of Bacteriology 186: 2928-2935.
C.D. Bayliss, T. van de Ven and E.R. Moxon (2002). Mutations in polI but not mutSLH destabilise Haemophilus influenzae tetranucleotide repeats. EMBO Jounal, 21:1465-1476.
X. De Bolle, C.D. Bayliss, D. Field, T. van de Ven, N.J. Saunders, D.W. Hood, and E.R. Moxon (2000). The length of a tetranucleotide repeat tract in Haemophilus influenzae determines the phase variation rate of a gene with homology to type III DNA methyltransferases. Molecular Microbiology, 35:211-222.
C.D. Bayliss (2009). Determinants of phase variation rate and the fitness implications of differing rates for bacterial pathogens and commensals. FEMS Microbiol Reviews. [Epub ahead of print].
E.R. Moxon, C.D. Bayliss and D.W. Hood (2007). Bacterial contingency loci: the role of simple sequence DNA repeats in bacterial adaptation. Annual Review of Genetics. 40:307-333.
C.D. Bayliss and E.R. Moxon (2005). Repeats and Variation in Pathogen Selection. Chapter in “The Implicit Genome” edited by Lynn Caparole. Oxford University Press.
C.D. Bayliss. K.M. Dixon and E.R. Moxon (2003). Simple sequence repeats (microsatellites): mutational mechanisms and contributions to bacterial pathogenesis. A meeting review. FEMS Immunol. Med. Microb. 40:11-19.
C.D. Bayliss and E.R. Moxon (2002). Hypermutation and bacterial adaptation. ASM News, 68:549-555.
C.D. Bayliss, D. Field and E.R. Moxon (2001). The simple sequence contingency loci of Haemophilus influenzae and Neisseria meningitidis. The Journal of Clinical Investigation, 107:657-662.
C.D. Bayliss, D. Field, X. De Bolle and E.R. Moxon (2000). The generation of diversity in Haemophilus influenzae. Response. Trends in Microbiology, 8:435-436.
The generation of genetic diversity is a central facet of evolution by natural selection. Pathogenic and commensal bacteria provide a rich model for studying the importance of genetic diversity and it’s rate of generation. These organisms are subject to stringent and adaptable responses from their hosts as well as competition from other microbes and attack by bacteriophages. Most bacterial species adapt to, or survive, these challenges through genetic variants and as a result multiple mechanisms have evolved in these organisms to generate genetic diversity. Characterisation of these mechanisms is critical for understanding bacterial pathogenesis and the evolution/spread of novel phenotypes such as antibiotic resistance but also reveals elemental aspects of the processes of natural selection. Tandem DNA repeat tracts (microsatellites) are hypermutable and enable the rapid generation of genetic variants. My research is focused on understanding the mechanistic basis for and consequences of mutations in tandem DNA repeat tracts.
Neisseria meningitidis (‘the meningococcus’) is the major causative agent of bacterial meningitis.
Meningococci are Gram –ve diplococci, which are usually found as commensals in the naso- and oropharynx of humans. The genomes of these bacteria contain a vast range of repetitive DNA with a range of known and potential functions. Tandem DNA repeat tracts are present within the promoters or reading frames of genes encoding surface structures or enzymes required for biosynthesis of surface structures. Mutations in these repeat tracts switch expression of genes ‘on’ and ‘off’, a process referred to as phase variation. These ‘phase variable’ changes in gene expression enable meningococci to escape immune responses and also impact on other phenotypes such as acquisition of iron and adhesion to host tissues. Experimental studies are being pursued using a range of in vitro models to investigate the effects on fitness of phase variation and of differences in the rate of mutation in the repeat tracts. Our recent collection of meningococcal carriage isolates has provided a new resource for investigations of natural changes in phase variable genes and the roles of other mechanisms for generation of genetic variation.
PhD projects with Neisseria meningitidis will focus on the following areas:-
• Phase variation-mediated escape of specific antibody responses
• Analysis of the functions and phase variation of iron acquisition systems
• Development of a reversible, selective assay of phase variation
• Examination of the extent of phase variable changes occurring in meningococcal genes during carriage
Campylobacter jejuni is frequently responsible for cases of food-borne gasteroenteritis. This Gram –ve spiral-shaped bacterial species is normally found as commensal in the gasterointestinal tracts of birds or other animals or as an environmental contaminant. The genomes of this species contains many genes subject to phase variation due to mutations in mononucleotide repeat tracts. Our recent development of a reporter system to measure the phase variation of these genes is facilitating studies of the factors controlling the rate of switching. The setting-up of protocols for detecting phase variants and for rapid analysis of repeat tract lengths is underpinning biological studies of the fitness impact of phase variation in this species.
PhD projects with Campylobacter jejuni will focus on the following areas:-
• Identification of the determinants of phase variation rate
• Investigation of the selection of phase variants in biological assays
• Computer modelling of the impact of phase variation on population diversity