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Chapter 6 : Genetics of Group A Streptococci

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Genetics of Group A Streptococci, Page 1 of 2

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Abstract:

Rapid progress has been made in recent years in the development of sophisticated techniques for genetic analysis in (the group A streptococcus). Much of this effort has been directed at the development of methods for the mutagenesis of known genes. A key element of any genetic system involves some system of genetic exchange between different bacterial hosts which allows the construction of an altered genome in the target host which can then be subjected to an analysis of its virulence phenotypes. Conjugative DNA transfer does occur in group A streptococci; however, this is restricted to the transfer of conjugative plasmids and conjugative transposons, and there is no evidence for mobilization of chromosomal markers. Much progress has also been made in the development of strategies for the identification of novel genes. It is likely that the widespread application of these techniques to the virulence properties of will enrich our understanding of streptococcal pathogenesis with insight at the molecular level and will help to establish and clarify the contributions of specific genes. Additional use and development of methods for analysis of gene expression and heterologous expression will continue and allow analyses of virulence factors at much higher levels of resolution than previously possible.

Citation: Hong Cho K, Caparon M. 2006. Genetics of Group A Streptococci, p 59-73. In Fischetti V, Novick R, Ferretti J, Portnoy D, Rood J (ed), Gram-Positive Pathogens, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816513.ch6

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Figures

Image of FIGURE 1
FIGURE 1

Strategy for allelic replacement mutagenesis using an omega interposon. The ΩKm-2 interposon contains a kanamycin-resistance gene that can be selected for in both gram-positive and gram-negative organisms. Additional features of ΩKm-2 include a cassettelike structure with several convenient restriction sites and strong transcription (open triangles) and translation (closed triangles) termination signals such that insertion of the element into a gene cloned in (top half of the figure) is strongly polar. The plasmid vector is converted to a linear molecule by digestion outside of the cloned streptococcal gene (vector DNA is represented by the nonstraight lines) and introduced into with selection for resistance to kanamycin. Recombination between homologous sequences (indicated by the lines between introduced DNA and chromosome) results in the replacement of the ΩKm-2-inactivated allele for the chromosomal allele (shown below the arrow). Abbreviations: E, RI; Sm, I; B, HI; H, dIII; Ev, RV.

Citation: Hong Cho K, Caparon M. 2006. Genetics of Group A Streptococci, p 59-73. In Fischetti V, Novick R, Ferretti J, Portnoy D, Rood J (ed), Gram-Positive Pathogens, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816513.ch6
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Image of FIGURE 2
FIGURE 2

Directed insertional mutagenesis of targeted genes. (A) A DNA segment internal to the targeted gene (shown by the box enclosed by wavy lines) is cloned onto an plasmid that cannot replicate in . The plasmid is introduced into an host as a circular molecule (top of figure) with selection for a resistance marker on the plasmid (ΩKm-2). A single homologous recombination event between the chromosome and the circular molecule (shown by the “X”) results in the integration of the plasmid into the chromosome and a partial duplication of the gene (the solid bars labeled A and B represent the duplicated segment) in which neither of the two copies is complete. (B) Generation of a polar insertion 39 to the target gene. If the segment of DNA cloned on the integrational plasmid contains sequences that include the 3′ terminus of the target gene, the resulting structure will also contain a partial duplication gene (the solid bars labeled A and B represent the duplicated segment), but in this case the 5′ copy will be intact and will now be flanked at its 3′ end by a polar element. This strategy can be used to test if the insertion generated in the target gene (see above) is polar on distal genes. (C) Mapping the -acting control regions of the target gene. In this strategy, the technique is modified by including different regions of DNA extending 5′ to the target gene. The plasmid is integrated into the target locus as described above, and the end product is also a partial duplication of the target gene (the solid bars labeled A and B represent the duplicated segment); however, it is the distal copy that is intact. If this region does not include the -acting control regions (represented by the broken arrow and the closed circle labeled P), the distal intact copy will not be expressed (scenario labeled 1). In contrast, if the cloned segment includes the -acting control regions, then the distal copy will be expressed (scenario labeled 2).

Citation: Hong Cho K, Caparon M. 2006. Genetics of Group A Streptococci, p 59-73. In Fischetti V, Novick R, Ferretti J, Portnoy D, Rood J (ed), Gram-Positive Pathogens, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816513.ch6
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Image of FIGURE 3
FIGURE 3

Construction of an in-frame deletion. Standard PCR-based methods are used to generate a deletion of the internal region of a copy of the target gene that has been cloned on an -streptococcal shuttle vector that is temperature sensitive for replication (). The deletion is constructed so as to maintain the reading frame of the gene (represented as the bent line connecting the 5′ region labeled A and the 3′ region labeled B). After its introduction into , growth at a temperature nonpermissive for replication of the plasmid with selection for the antibiotic-resistant determinant of the plasmid () selects for chromosomes in which the plasmid has integrated by homologous recombination (X). The two regions of homology flanking the deletion are represented by the solid and gray bars labeled A and B. Recombination between the A regions is shown, and the product is shown below the first arrow. A second homologous recombination event can occur between the 5′ homologous regions (labeled A) or the 3′ homologous regions (labeled B), which results in excision of the plasmid and either restoration of the wild-type structure or replacement by the deletion allele (these products are illustrated below the second set of arrows). Growth at a temperature permissive for replication of the plasmid enriches for chromosomes from which the plasmid has been excised. Presence of the wild-type or deletion allele in any one isolate is easily determined by assay for the unique restriction site engineered into the deletion allele (indicated by the R above the bent line).

Citation: Hong Cho K, Caparon M. 2006. Genetics of Group A Streptococci, p 59-73. In Fischetti V, Novick R, Ferretti J, Portnoy D, Rood J (ed), Gram-Positive Pathogens, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816513.ch6
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Image of FIGURE 4
FIGURE 4

Transposon mutagenesis of . The several transposons that have been used for mutagenesis of are shown. Antibiotic resistance genes are represented by the gray bars; transposon ends and/or terminal inverted repeats are shown in black; genes that are essential for transposition are shown by white bars; and genes that are nonessential for transposition are represented by the striped bars. Tn (GenBank accession no. U09422) is the prototype conjugative transposon and contains at least 24 different open reading frames. Of these, one is required for resistance to tetracycline, two are essential for transposition, and the rest are likely involved in conjugal transfer. Tn-LTV3 is a highly engineered derivative of the Tn-like transposon Tn. This element transposes via a replicative mechanism and has been modified to include a promoterless reporter gene to generate random transcriptional fusions and an ColE1 plasmid origin of replication to facilitate the cloning and analysis of inactivated loci. TnSpc is a derivative of the Tn-like transposon Tn. This element transposes via a cut-and-paste mechanism and consists of the left and right inverted repeats and transposase of IS and a spectinomycin resistance gene.

Citation: Hong Cho K, Caparon M. 2006. Genetics of Group A Streptococci, p 59-73. In Fischetti V, Novick R, Ferretti J, Portnoy D, Rood J (ed), Gram-Positive Pathogens, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816513.ch6
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Image of FIGURE 5
FIGURE 5

The structure of TnFuZ. The element contains the left and right inverted repeats (IR and IR, respectively), the transposase () of IS, and the kanamycin resistance determinant contained on Ωkm-2. The gene encoding the alkaline phosphatase () was altered by removal of the region that encoded its signal sequence, and the modified gene (*) was introduced into the element as shown. Abbreviations: C, I; Ev, RV; Nc, I; P, I; S, I; Sm, I. A slash indicates a junction of two restriction fragments joined during construction of the element, and restriction sites enclosed by parentheses are inactive.

Citation: Hong Cho K, Caparon M. 2006. Genetics of Group A Streptococci, p 59-73. In Fischetti V, Novick R, Ferretti J, Portnoy D, Rood J (ed), Gram-Positive Pathogens, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816513.ch6
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Image of FIGURE 6
FIGURE 6

The structure of pMOD-2::Ω containing the novel transposon TmErm. The transposon TmErm contains the right and left inverted repeats (mosaic end, ME) modified from the inverted repeats of Tn, and an erythromycin resistance marker (Ω). To apply the transposome mutagenesis to , the DNA fragment containing transposon TmErm was purified after digestion with II. Thus, the ampicillin resistance determinant contained on pMOD-2::Ωwas removed before the transposome mutagenesis. The purified transposon TmErm was then reacted with a transposase (EZ::TN, Epicentre Technologies) in vitro to form the transposome that is then used to transform using electroporation. Several restriction sites in the plasmid are indicated: P, II; Ba, HI; Bs, I.

Citation: Hong Cho K, Caparon M. 2006. Genetics of Group A Streptococci, p 59-73. In Fischetti V, Novick R, Ferretti J, Portnoy D, Rood J (ed), Gram-Positive Pathogens, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816513.ch6
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Image of FIGURE 7
FIGURE 7

A chimeric secreted alkaline phosphatase reporter gene. The plasmid pABG5 is a pWV01-based -streptococcal shuttle vector whose genes encode resistance to chloramphenicol () and kanamycin (). The plasmid contains a promoterless reporter gene formed by the fusion of the N-terminal region of the cell wall-associated protein F () to the enzymatic domain of the enterococcal alkaline phosphatase (). Because the chimeric protein (secreted protein F-PhoZ reporter, or PhoZF) lacks the C-terminal cell wall attachment domain of protein F and the N-terminal lipoprotein tethering domain of PhoZ, it is freely secreted from the cell. The PhoZF chimera retains the enzymatic activity of PhoZ and is easily quantified in culture supernatants. Restriction sites for HI and RI can be used to place the promoter of interest in an orientation to direct transcription of , which is then translated using the ribosome-binding site of (RBS). The plasmid pABG5 contains the promoter, which confers high-level expression.

Citation: Hong Cho K, Caparon M. 2006. Genetics of Group A Streptococci, p 59-73. In Fischetti V, Novick R, Ferretti J, Portnoy D, Rood J (ed), Gram-Positive Pathogens, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816513.ch6
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