Professor Christopher D. Bayliss

Dr Chris Bayliss
Professor in Bacterial Genetics

Tel: +44 (0)116 252 3465
Fax: +44 (0)116 252 3378





Personal details

BSc, PhD

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.

In 2012, I became a Lecturer and in 2017 was promoted to a Reader in Bacterial Genetics within the newly renamed Department of Genetics and Genome Biology. I lead an active research group with interested in understanding hypermutable DNA sequences in bacterial pathogens such as Neisseria meningitidis, Haemophilus influenzae and Campylobacter jejuni.

Postgraduate teaching

Undergraduate Area of Teaching

  • Microbial genetics and genomics
  • Infection and infectious disease
  • Vaccinology

Other responsibilities

  • Genetic Modification Sub-Committee member
  • Outreach: talks to Meningitis Research Foundation



Oldfield NJ, Cayrou C, AlJannat MAK, Al-Rubaiawi AAA, Green LR, Dada S, Steels OD, Stirrup C, Wanford J, Atwah BAY, Bayliss CD, Turner DPJ. (2017). Rise in Group W Meningococcal Carriage in University Students, United Kingdom. Emerg Infect Dis. 2017 Jun;23(6):1009-1011. PMID: 28518025

Aidley J, Rajopadhye S, Akinyemi NM, Lango-Scholey L, Bayliss CD. (2017). Nonselective Bottlenecks Control the Divergence and Diversification of Phase-Variable Bacterial Populations. MBio. 8. pii: e02311-16.

Turner DP, Oldfield NJ, Bayliss CD. (2017). University vaccine campaign increases meningococcal ACWY vaccine coverage. Public Health. 145:1-3. PMID: 28359377

Lango-Scholey L, Aidley J, Woodacre A, Jones MA, Bayliss CD. (2016) High Throughput Method for Analysis of Repeat Number for 28 Phase Variable Loci of Campylobacter jejuni Strain NCTC11168. PLoS One. 2016 Jul 28;11(7):e0159634.

Bayliss CD, Morrissey JA, Borrow R (2016) Men B: lack of coverage or vaccine failure? Lancet, 387:531-2.

Anjum A, Brathwaite KJ, Aidley J, Connerton PL, Cummings NJ, Parkhill J, Connerton I, Bayliss CD. (2016). Phase variation of a Type IIG restriction-modification enzyme alters site-specific methylation patterns and gene expression in Campylobacter jejuni strain NCTC11168. Nucleic Acids Res., 44:4581-94.

Oldfield NJ, Harrison OB, Bayliss CD, Maiden MC, Ala'Aldeen DA, Turner DP (2016) Genomic Analysis of Serogroup Y Neisseria meningitidis Isolates Reveals Extensive Similarities Between Carriage-Associated and Disease-Associated Organisms. J Infect Dis., 213:1777-85

Alamro M, Bidmos FA, Chan H, Oldfield NJ, Newton E, Bai X, Aidley J, Care R, Mattick C, Turner DP, Neal KR, Ala'aldeen DA, Feavers I, Borrow R, Bayliss CD (2014). Phase variation mediates reductions in expression of surface proteins during persistent meningococcal carriage. Infect. Imm. 82: 2472-84 (PMID:24686058).

Lucidarme J, Findlow J, Chan H, Feavers IM, Gray SJ, Kaczmarski EB, Parkhill J, Bai X, Borrow R, Bayliss CD (2013). The distribution and 'in vivo' phase variation status of haemoglobin receptors in invasive meningococcal serogroup B disease: genotypic and phenotypic analysis. PLoS ONE 8(9): e76932.doi:101371 (PMID:24098814).

Palmer ME, Lipsitch M, Moxon ER, Bayliss CD. (2013) Broad conditions favor the evolution of phase-variable loci. MBio., 4:e00430-12. doi: 10.1128/mBio.00430-12.

Tauseef I, Ali YM, Bayliss CD. (2013). Phase variation of PorA, a major outer membrane protein, mediates escape of bactericidal antibodies by Neisseria meningitidis. Infect Immun. 81:1374-80.

Bayliss CD, Bidmos FA, Anjum A, Manchev VT, Richards RL, Grossier JP, Wooldridge KG, Ketley JM, Barrow PA, Jones MA, Tretyakov MV (2012). Phase variable genes of Campylobacter jejuni exhibit high mutation rates and specific mutational patterns but mutability is not the major determinant of population structure during host colonization. Nucl. Acids Res. 40:5876-89.

Bidmos FA, Neal KR, Oldfield NJ, Turner DP, Ala'Aldeen DA, Bayliss CD (2011). Persistence, replacement and rapid clonal expansion of meningococcal carriage isolates in a 2008 university student cohort. Journal Clin. Micro. 49: 506-512.

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

Neisseria meningitidis (‘the meningococcus’) is the major causative agent of bacterial meningitis.

Neisseria Meningitidis
Neisseria Meningitidis

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

Campylobacter Jejuni
Campylobacter Jejuni

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

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Contact Details

Department of Genetics
University of Leicester

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United Kingdom

Tel: +44 (0)116 252 3374
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Professor Jacqui Shaw

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