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Chapter 5 : Genome Plasticity in and : Impact on Host Cell Exploitation

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Abstract:

This chapter starts with a description of the general characteristics of the genome sequences of and . It then highlights the characteristic features and common traits of the two main human-pathogenic Legionella species. Emphasis is given to putative virulence and life cycle-related functions. In the second part, the focus is on the comparison of these genome sequences, in order to learn about the plasticity of the genomes and the possible mechanisms involved. In the third part, the possible evolution of the identified virulence factors are analyzed and discussed. Finally, future perspectives in genomics are presented. NSW 150 encodes four T4SS, a rather exceptional number and D-4968 encodes two T4SS. The authors found that IcmE/DotG of (1,525 amino acids) is 477 amino acids larger than that of (1,048 amino acids). Most of the T4SS are located on regions of genome plasticity; some even show plasticity on the gene/protein level, as shown above for DotG. The authors undertook a phylogenetic analysis for the protein Llo2643, which contains PPR repeats, a protein family typically present in plants. In the last few years, genome analyses, as well as comparative and functional genomics, have demonstrated that genome plasticity plays a major role in differences in host cell exploitation and niche adaptation of .

Citation: Gomez Valero L, Rusniok C, Buchrieser C. 2012. Genome Plasticity in and : Impact on Host Cell Exploitation, p 58-83. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch5

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Bacteria and Archaea
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Bacterial Proteins
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Type II Secretion System
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Image of FIGURE 1
FIGURE 1

Synteny plot of the chromosomes of Paris, Lens, Corby, and Philadelphia-1. The plot was created with the MUMmer software package.

Citation: Gomez Valero L, Rusniok C, Buchrieser C. 2012. Genome Plasticity in and : Impact on Host Cell Exploitation, p 58-83. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch5
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Image of FIGURE 2
FIGURE 2

Diagram showing the core genome and the unique gene complement of Paris, Lens, Philadelphia-1, and Corby. Orthologous genes were defined by reciprocal best-match FASTA comparisons. The threshold was set to a minimum of 80% sequence identities and a ratio of the length of 0.75 to 1.33.

Citation: Gomez Valero L, Rusniok C, Buchrieser C. 2012. Genome Plasticity in and : Impact on Host Cell Exploitation, p 58-83. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch5
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Image of FIGURE 3
FIGURE 3

Synteny plot of the chromosomes of Paris and NSW 150. The plot was created with the MUMmer software package.

Citation: Gomez Valero L, Rusniok C, Buchrieser C. 2012. Genome Plasticity in and : Impact on Host Cell Exploitation, p 58-83. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch5
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Image of FIGURE 4
FIGURE 4

Phylogenetic tree showing the relationship of the four sequenced strains based on the sequence. The tree was constructed using the neighbor-joining method in MEGA. Numbers at branching nodes are percentages of 1,000 bootstrap replications.doi:10.1128/9781555817213.ch05f04

Citation: Gomez Valero L, Rusniok C, Buchrieser C. 2012. Genome Plasticity in and : Impact on Host Cell Exploitation, p 58-83. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch5
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Image of FIGURE 5
FIGURE 5

Alignment of the chromosomal regions of and encoding the Dot/Icm type 4 secretion system genes. (A) The comparison shows that all genes are highly conserved (47% to 92% identity) between Paris and . Red, conserved genes; blue, specific genes; green arrows, -specific genes. (B) Self matrix of DotG of and .

Citation: Gomez Valero L, Rusniok C, Buchrieser C. 2012. Genome Plasticity in and : Impact on Host Cell Exploitation, p 58-83. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch5
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Image of FIGURE 6
FIGURE 6

Phylogenetic tree of a multiple-sequence comparison of SPL proteins present in eukaryotic and prokaryotic genomes. Phylogenetic reconstruction was done with MEGA, using the neighbor-joining method. Numbers indicate bootstrap values after 1,000 bootstrap replicates. The red lines indicate the sequences that are embedded in the eukaryotic clade. The bar at the bottom represents the estimated evolutionary distance.

Citation: Gomez Valero L, Rusniok C, Buchrieser C. 2012. Genome Plasticity in and : Impact on Host Cell Exploitation, p 58-83. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch5
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Image of FIGURE 7
FIGURE 7

Phylogenetic tree of the protein Llo2643 and its homologues after a BlastP search. The tree was constructed by the neighbor-joining method using the program MEGA. The red lines indicate the sequences that are close to sequences derived from plant genomes. Numbers indicate bootstrap support for nodes from 1,000 neighbor-joining bootstrap replicates. The bar at the bottom represents the estimated evolutionary distance.

Citation: Gomez Valero L, Rusniok C, Buchrieser C. 2012. Genome Plasticity in and : Impact on Host Cell Exploitation, p 58-83. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch5
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Tables

Generic image for table
TABLE 1

Complete genomes obtained by classical Sanger sequencing

Citation: Gomez Valero L, Rusniok C, Buchrieser C. 2012. Genome Plasticity in and : Impact on Host Cell Exploitation, p 58-83. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch5
Generic image for table
TABLE 2

Complete and draft genomes of obtained by classical sequencing and new generation sequencing

Citation: Gomez Valero L, Rusniok C, Buchrieser C. 2012. Genome Plasticity in and : Impact on Host Cell Exploitation, p 58-83. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch5
Generic image for table
TABLE 3

Distribution of known and predicted Dot/Icm substrates of in

Citation: Gomez Valero L, Rusniok C, Buchrieser C. 2012. Genome Plasticity in and : Impact on Host Cell Exploitation, p 58-83. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch5
Generic image for table
TABLE 4

Putative new type IV secretion substrates specific for

Citation: Gomez Valero L, Rusniok C, Buchrieser C. 2012. Genome Plasticity in and : Impact on Host Cell Exploitation, p 58-83. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch5

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