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Category: Microbial Genetics and Molecular Biology; Genomics and Bioinformatics
Selfish Elements and Self-Defense in the Enterococci, Page 1 of 2
< Previous page | Next page > /docserver/preview/fulltext/10.1128/9781555817213/9781555817084_Chap08-1.gif /docserver/preview/fulltext/10.1128/9781555817213/9781555817084_Chap08-2.gifAbstract:
This chapter reviews the genome plasticity that has led to distinct subpopulations of enterococci, as well as the evidence for loss of genome defenses as precipitating events in their emergence. It presents evidence as it currently exists describing the role of genome plasticity in the virulence and persistence of hospital-adapted, multidrug-resistant enterococcal lineages. It also highlights the mechanistic and comparatively unappreciated role that loss of endogenous genome defenses, such as restriction modification and clustered, regularly interspaced, short palindromic repeats (CRISPR) systems, may have played in the emergence of these lineages. To the authors knowledge, the extent to which insertion sequence (IS) element inactivation of chromosomal genes contributes to the success of enterococci as pathogens has not been explored. However, there is evidence that intragenomic recombination at IS elements has contributed substantially to genome plasticity of the enterococci. The chapter focuses on genome defense mechanisms in the enterococci, including restriction-modification and CRISPR. Much work remains to be done before understanding whether and how genome defense mechanisms influence enterococcal ecology and evolution.
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Phylogenetic relatedness and variable trait profile of diverse E. faecalis isolates. Shown is the MLST dendrogram for 106 E. faecalis strains, aligned with their capsule type (CPS), date of isolation, isolation source, PAI fragment content, antibiotic resistance profile, and phenotypic auxiliary traits. PAI fragments are designated A through F, and a red letter B indicates that the strain can conjugatively transfer cytolysin to other E. faecalis strains. Antibiotic resistance shown includes tetracycline (TL, tetL; TM, tetM), erythromycin (E, ermB), gentamicin (G), chloramphenicol (C, cat), ampicillin (A, blaZ), and vancomycin (VA, vanA; VB, vanB) resistance. Auxiliary traits are cytolysin production (CYL), conjugated bile salt hydrolase production (CBH), and gelatinase production (GEL). Reprinted from PLoS One ( McBride et al., 2007 ).
Phylogenetic relatedness and variable trait profile of diverse E. faecalis isolates. Shown is the MLST dendrogram for 106 E. faecalis strains, aligned with their capsule type (CPS), date of isolation, isolation source, PAI fragment content, antibiotic resistance profile, and phenotypic auxiliary traits. PAI fragments are designated A through F, and a red letter B indicates that the strain can conjugatively transfer cytolysin to other E. faecalis strains. Antibiotic resistance shown includes tetracycline (TL, tetL; TM, tetM), erythromycin (E, ermB), gentamicin (G), chloramphenicol (C, cat), ampicillin (A, blaZ), and vancomycin (VA, vanA; VB, vanB) resistance. Auxiliary traits are cytolysin production (CYL), conjugated bile salt hydrolase production (CBH), and gelatinase production (GEL). Reprinted from PLoS One ( McBride et al., 2007 ).
E. faecalis OG1RF CRISPR loci. (A) Diagram of CRISPR loci identified in the OG1RF genome by Bourgogne et al. (2008) . Homologues of E. faecalis V583 genes are shown in black with appropriate V583 locus numbers. CRISPR-associated genes (cas) genes are specific to OG1RF and are shown in red. An ORF that lacks homology to known cas genes and is also specific to OG1RF was predicted to occur downstream of the CRISPR1 repeat-spacer array ( Bourgogne et al., 2008 ). Vertical black lines represent 36-bp repeat sequences of CRISPR repeat-spacer arrays. (B) An OG1RF CRISPR spacer is homologous to a mobile element present in the V583 genome. Shown is the 30-bp OG1RF CRISPR1 spacer 3 sequence aligned with a homologous sequence in V583. Homologous nucleotides are in bold and underlined. The V583 sequence is located in an intergenic region between the ORFs EF2528 and EF2529; this region is found within a predicted integrated plasmid on the V583 genome (EF2512 to EF2545 [ McBride et al., 2007 ]). Components of the figure are not drawn to scale.
E. faecalis OG1RF CRISPR loci. (A) Diagram of CRISPR loci identified in the OG1RF genome by Bourgogne et al. (2008) . Homologues of E. faecalis V583 genes are shown in black with appropriate V583 locus numbers. CRISPR-associated genes (cas) genes are specific to OG1RF and are shown in red. An ORF that lacks homology to known cas genes and is also specific to OG1RF was predicted to occur downstream of the CRISPR1 repeat-spacer array ( Bourgogne et al., 2008 ). Vertical black lines represent 36-bp repeat sequences of CRISPR repeat-spacer arrays. (B) An OG1RF CRISPR spacer is homologous to a mobile element present in the V583 genome. Shown is the 30-bp OG1RF CRISPR1 spacer 3 sequence aligned with a homologous sequence in V583. Homologous nucleotides are in bold and underlined. The V583 sequence is located in an intergenic region between the ORFs EF2528 and EF2529; this region is found within a predicted integrated plasmid on the V583 genome (EF2512 to EF2545 [ McBride et al., 2007 ]). Components of the figure are not drawn to scale.
Examples of enterococcal plasmids that have served as models for understanding their contribution to virulence and antibiotic resistance transmission
Examples of enterococcal plasmids that have served as models for understanding their contribution to virulence and antibiotic resistance transmission
Putative restriction-modification systems in complete E. faecalis genomes
Putative restriction-modification systems in complete E. faecalis genomes