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Chapter 8 : Selfish Elements and Self-Defense in the Enterococci

Authors: Kelli L. Palmer1, Michael S. Gilmore2
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Affiliations: 1: Schepens Eye Research Institute, 20 Staniford St., Boston, MA 02144; 2: Schepens Eye Research Institute, 20 Staniford St., Boston, MA 02144
Content Type: Monograph
Publication Year: 2012

Category: Microbial Genetics and Molecular Biology; Genomics and Bioinformatics

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Abstract:

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.

Citation: Palmer K, Gilmore M. 2012. Selfish Elements and Self-Defense in the Enterococci, p 125-140. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch8
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Selfish Elements and Self-Defense in the Enterococci
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Citation: Palmer K, Gilmore M. 2012. Selfish Elements and Self-Defense in the Enterococci, p 125-140. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch8
/content/10.1128/9781555817213.chap8.fig8-1
FIGURE 1

Phylogenetic relatedness and variable trait profile of diverse isolates. Shown is the MLST dendrogram for 106 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 strains. Antibiotic resistance shown includes tetracycline (TL, ; TM, ), erythromycin (E, ), gentamicin (G), chloramphenicol (C, ), ampicillin (A, ), and vancomycin (VA, ; VB, ) resistance. Auxiliary traits are cytolysin production (CYL), conjugated bile salt hydrolase production (CBH), and gelatinase production (GEL). Reprinted from ( ).

10.1128/9781555817213/fig8-1_thmb.gif
10.1128/9781555817213/fig8-1.gif
Image of FIGURE 1
FIGURE 1

Phylogenetic relatedness and variable trait profile of diverse isolates. Shown is the MLST dendrogram for 106 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 strains. Antibiotic resistance shown includes tetracycline (TL, ; TM, ), erythromycin (E, ), gentamicin (G), chloramphenicol (C, ), ampicillin (A, ), and vancomycin (VA, ; VB, ) resistance. Auxiliary traits are cytolysin production (CYL), conjugated bile salt hydrolase production (CBH), and gelatinase production (GEL). Reprinted from ( ).

Citation: Palmer K, Gilmore M. 2012. Selfish Elements and Self-Defense in the Enterococci, p 125-140. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch8
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/content/10.1128/9781555817213.chap8.fig8-2
FIGURE 2

OG1RF CRISPR loci. (A) Diagram of CRISPR loci identified in the OG1RF genome by . Homologues of V583 genes are shown in black with appropriate V583 locus numbers. CRISPR-associated genes () genes are specific to OG1RF and are shown in red. An ORF that lacks homology to known genes and is also specific to OG1RF was predicted to occur downstream of the CRISPR1 repeat-spacer array ( ). 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 [ ]). Components of the figure are not drawn to scale.

10.1128/9781555817213/fig8-2_thmb.gif
10.1128/9781555817213/fig8-2.gif
Image of FIGURE 2
FIGURE 2

OG1RF CRISPR loci. (A) Diagram of CRISPR loci identified in the OG1RF genome by . Homologues of V583 genes are shown in black with appropriate V583 locus numbers. CRISPR-associated genes () genes are specific to OG1RF and are shown in red. An ORF that lacks homology to known genes and is also specific to OG1RF was predicted to occur downstream of the CRISPR1 repeat-spacer array ( ). 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 [ ]). Components of the figure are not drawn to scale.

Citation: Palmer K, Gilmore M. 2012. Selfish Elements and Self-Defense in the Enterococci, p 125-140. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch8
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Tables

Selfish Elements and Self-Defense in the Enterococci
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Citation: Palmer K, Gilmore M. 2012. Selfish Elements and Self-Defense in the Enterococci, p 125-140. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch8
/content/10.1128/9781555817213.chap8.tab8-1
TABLE 1

Examples of enterococcal plasmids that have served as models for understanding their contribution to virulence and antibiotic resistance transmission

10.1128/9781555817213/tab8-1_thmb.gif
10.1128/9781555817213/tab8-1.gif
Generic image for table
TABLE 1

Examples of enterococcal plasmids that have served as models for understanding their contribution to virulence and antibiotic resistance transmission

Citation: Palmer K, Gilmore M. 2012. Selfish Elements and Self-Defense in the Enterococci, p 125-140. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch8
/content/10.1128/9781555817213.chap8.tab8-2
TABLE 2

Putative restriction-modification systems in complete genomes

10.1128/9781555817213/tab8-2_thmb.gif
10.1128/9781555817213/tab8-2.gif
Generic image for table
TABLE 2

Putative restriction-modification systems in complete genomes

Citation: Palmer K, Gilmore M. 2012. Selfish Elements and Self-Defense in the Enterococci, p 125-140. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch8

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