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Lipopolysaccharide Phase Variation in Haemophilus and Neisseria
Published in Helmut Brade, Steven M. Opal, Stefanie N. Vogel, David C. Morrison, Endotoxin in Health and Disease, 2020
Derek W. Hood, E. Richard Moxon
The basis for the mechanism by which most characterized LPS phase variation is exerted is the presence of short nucleotide repeats situated within biosynthetic genes. All reiterated short nucleotide repeats are presumed to vary through a process related to slipped-strand mispairing (20). Polymerase slippage during nucleic acid replication is recA independent and results in loss or gain of a repeat unit. This phase-variation mechanism is distinct from other types of genetic antigenic variation that occur in pathogenic bacteria: the pilin genes of Neisseria vary by recombination between a functional and many silent copies of the major structural gene (21); surface proteins of gram-positive cocci contain large repetitive tracts within the genes, which are altered by recombinational events (22). In mucosal pathogens, the phase-variable expression of LPS is known to be promoted by tetranucleotide repeats in H. influenzae and by mononucleotide repeats in N. meningitidis and N. gonorrhoeae. Reports of other organisms displaying LPS capable of phase variation include Franciscella, Chlamydia, Coxiella, Helicobacter, and Bordetella species, but the nature and mechanisms of these variations are not fully understood.
Flagellum and toxin phase variation impacts intestinal colonization and disease development in a mouse model of Clostridioides difficile infection
Published in Gut Microbes, 2022
Dominika Trzilova, Mercedes A. H. Warren, Nicole C. Gadda, Caitlin L. Williams, Rita Tamayo
Many bacterial species employ phase variation to generate phenotypic heterogeneity within a clonal population. Bacteria frequently encounter selective pressures in their environment, and phenotypic heterogeneity helps ensure survival by creating subpopulations that are differentially equipped to overcome these pressures.1 Phase variation typically affects the production of surface factors that directly interface with the bacterium’s environment, such as flagella, pili, and exopolysaccharides. Both mucosal pathogens and commensal species employ phase variation to balance the fitness advantages conferred by these structures with the costs of producing them; in a host environment, the ability to phase vary can promote immune evasion and persistence in the host.2 Phase variation can be achieved by multiple epigenetic and genetic mechanisms, including DNA modification by methylation, slipped-strand mispairing, homologous recombination, and site-specific recombination.1,3
Serogroup A meningococcal conjugate vaccines: building sustainable and equitable vaccine strategies
Published in Expert Review of Vaccines, 2020
Amy C. Sherman, David S. Stephens
With advancements in molecular pathogenesis and whole genome sequencing, additional outer membrane surface structures and specific genotypes (clonal complexes such as ST-11, ST-5, ST-23) have also been linked to meningococcal virulence. The meningococcus has a single chromosome of 2.1–2.3 mega bases. Multilocus sequence typing (MLST), which involves DNA sequencing of portions of seven housekeeping genes and whole genome sequencing are now the tools utilized for molecular epidemiology and characterization of N. meningitidis [11] and are also used to identify molecular markers such as capsular switching. The first whole genome sequences were of serogroup B (MC58, ST-32) and serogroup A (Z2491, ST-4) strains and were reported in 2000 [i]. N. meningitidis has the capacity to acquire, at high frequency, DNA through horizontal gene transfer and homologous recombination. In addition, there are several mechanisms that have been defined (e.g. genetic slipped strand mispairing) that allow the pathogen to alter its antigenic profile. This variability does create challenges for meningococcal vaccine development, vaccine efficacy, and long-term effectiveness. For example, the allelic replacement of capsular biosynthesis genes, e.g. capsular switching [12,13], can reduce meningococcal vaccine effectiveness and influence vaccine strategies.
Genotyping comparison of Mycobacterium leprae isolates by VNTR analysis from nasal samples in a Brazilian endemic region
Published in Pathogens and Global Health, 2018
Luana Nepomueceno Costa Lima, Cristiane Cunha Frota, Phillip Noel Suffys, Amanda Nogueira Brum Fontes, Rosa Maria Salani Mota, Rosa Livia Freitas Almeida, Maria Araci de Andrade Pontes, Heitor de Sá Gonçalves, Carl Kendall, Ligia Regina Sansigolo Kerr
The conventional epidemiology of leprosy has be improved by strain genotyping tools. The isolates differentiation approach using molecular markers are useful to distinguish different strains of the leprosy bacilli. Variable number tandem repeat (VNTR) provides data about the pattern of variation in the Mycobacterium leprae genome [3–5]. The VNTR typing tool is based on the number of repetitive sequences in polymorphic micro- and mini-satellite regions of the bacteria [6]. Some polymorphic loci are suitable for identifying genotypes according to the discriminatory capacity, stability, and reproducibility. There is considerably more variation in repeat numbers at VNTR locus than in non-repetitive DNA sequences, because length-altering mutations due to slipped-strand mispairing occur at a much higher rate than the inherent DNA substitution or mutation frequency of DNA polymerase [7,8].