Bayliss, Christopher D. - University of Leicester

个人简介

Chris Bayliss grew up in rural villages of Surrey and South Yorkshire. After completing his first degree in Microbiology (Aberystwyth, University College of Wales), he went on to clone and sequence a dsRNA virus of chickens as part of his PhD at Houghton Poultry Research Institute in Cambridgeshire. He 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. In 1997, Chris 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 seven-years, he moved to the University of Nottingham where he held a Wellcome Trust Value in People Award. Chris obtained an RCUK Research Fellow in the Department of Genetics, University of Leicester in 2007 and leads an active research group with an interest in hypermutable DNA sequences.

研究领域

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.

近期论文

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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.