The minimal mobile element

Microbiology (Impact Factor: 2.56). 01/2003; 148(Pt 12):3756-60. DOI: 10.1099/00221287-148-12-3756
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Available from: Lori A S Snyder
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    • "Homologous recombination at the conserved flanking genes would account for this phenomenon whereby gene organization was identical between distantly related genomes but different between the closely related ST60 genomes. These regions displayed characteristics of minimal mobile elements , which were defined as variable regions among the closest relatives in sequence composition and gene content between specific conserved flanking genes (Saunders and Snyder 2002; Snyder et al. 2007). Among the nine regions, only the glnD-guaB region (fig. "
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    ABSTRACT: The study of genetic and phenotypic variation is fundamental for understanding the dynamics of bacterial genome evolution and untangling the evolution and epidemiology of bacterial pathogens. Neisseria meningitidis (Nm) is among the most intriguing bacterial pathogens in genomic studies due to its dynamic population structure and complex forms of pathogenicity. Extensive genomic variation within identical clonal complexes in Nm has been recently reported and suggested to be the result of homologous recombination, but the extent to which recombination contributes to genomic variation within identical clonal complexes has remained unclear. In this study, we sequenced two Nm strains of identical serogroup (C) and multi-locus sequence type (ST60), and conducted a systematic analysis with an additional 34 Nm genomes. Our results revealed that all gene content variation between the two ST60 genomes was introduced by homologous recombination at the conserved flanking genes, and 94.25% or more of sequence divergence was caused by homologous recombination. Recombination was found in genes associated with virulence factors, antigenic outer membrane proteins, and vaccine targets, suggesting an important role of homologous recombination in rapidly altering the pathogenicity and antigenicity of Nm. Recombination was also evident in genes of the restriction and modification systems, which may undermine barriers to DNA exchange. In conclusion, homologous recombination can drive both gene content variation and sequence divergence in Nm. These findings shed new light on the understanding of the rapid pathoadaptive evolution of Nm and other recombinogenic bacterial pathogens.
    Full-text · Article · Jul 2013 · Genome Biology and Evolution
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    • "Of the 5 previously reported genes disrupted by CREE insertion [8,21,22], 4 are associated with CREE in these two gonococcal genome sequences (Table 3). In the case of NMA2121, this CDS is not present in strain FA1090 as it is part of a Minimal Mobile Element [22,39,40], which facilitates horizontal exchange of gene cassettes between genome sequences. "
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    ABSTRACT: The Correia Repeat Enclosed Element (CREE) of the Neisseria spp., with its inverted repeat and conserved core structure, can generate a promoter sequence at either or both ends, can bind IHF, and can bind RNase III and either be cleaved by it or protected by it. As such, the presence of this element can directly control the expression of adjacent genes. Previous work has shown differences in regulation of gene expression between neisserial strains and species due to the presence of a CREE. These interruptions perhaps remove the expression of CREE-associated genes from ancestral neisserial regulatory networks. Analysis of the chromosomal locations of the CREE in Neisseria gonorrhoeae strain FA1090 and N. gonorrhoeae strain NCCP11945 has revealed that most of the over 120 copies of the element are conserved in location between these genome sequences. However, there are some notable exceptions, including differences in the presence and sequence of CREE 5' of copies of the opacity protein gene opa, differences in the potential to bind IHF, and differences in the potential to be cleaved by RNase III. The presence of CREE insertions in one strain relative to the other, CREE within a prophage region, and CREE disrupting coding sequences, provide strong evidence of mobility of this element in N. gonorrhoeae. Due to the previously demonstrated role of these elements in altering transcriptional control and the findings from comparing the two gonococcal genome sequences, it is suggested that regulatory differences orchestrated by CREE contribute to the differences between strains and also between the closely related yet clinically distinct species N. gonorrhoeae, Neisseria meningitidis, and Neisseria lactamica.
    Full-text · Article · Mar 2009 · BMC Genomics
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    • "We had instead chosen to evaluate the gene complements of 12 MLST analyzed strains to assess the genes present in N. lactamica. To this data we added one other N. lactamica strain that we had used previously [11,19]. In addition, our study sought to identify genes that are present in N. lactamica, not those that are absent from the commensal species, as was the goal of the Stabler et al [17] study. "
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    ABSTRACT: Neisseria meningitidis causes the life-threatening diseases meningococcal meningitis and meningococcal septicemia. Neisseria gonorrhoeae is closely related to the meningococcus, but is the cause of the very different infection, gonorrhea. A number of genes have been implicated in the virulence of these related yet distinct pathogens, but the genes that define and differentiate the species and their behaviours have not been established. Further, a related species, Neisseria lactamica is not associated with either type of infection in normally healthy people, and lives as a harmless commensal. We have determined which of the genes so far identified in the genome sequences of the pathogens are also present in this non-pathogenic related species. Thirteen unrelated strains of N. lactamica were investigated using comparative genome hybridization to the pan-Neisseria microarray-v2, which contains 2845 unique gene probes. The presence of 127 'virulence genes' was specifically addressed; of these 85 are present in N. lactamica. Of the remaining 42 'virulence genes' only 11 are present in all four of the sequenced pathogenic Neisseria. Assessment of the complete dataset revealed that the vast majority of genes present in the pathogens are also present in N. lactamica. Of the 1,473 probes to genes shared by all four pathogenic genome sequences, 1,373 hybridize to N. lactamica. These shared genes cannot include genes that are necessary and sufficient for the virulence of the pathogens, since N. lactamica does not share this behaviour. This provides an essential context for the interpretation of gene complement studies of the pathogens.
    Full-text · Article · Feb 2006 · BMC Genomics
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