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Chapter 21 : Mobile DNA in the Pathogenic

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Abstract:

The majority of species in the genus are commensal bacteria that colonize mucosal surfaces. The two pathogenic species, (the gonococcus) and (the meningococcus), are the causative agent of gonorrhea and the primary cause of bacterial meningitis in young adults, respectively. Both organisms are strict human pathogens with no known environmental reservoirs that have evolved from commensal organisms within the human population ( ). The study of the is important for public health reasons, but also provides a defined system to study evolution of two highly related organisms that cause distinct diseases. One unique aspect of the pathogenic is the presence of sophisticated genetic systems that contribute to pathogenesis. The processes of DNA transformation and pilin antigenic variation will be discussed in this chapter.

Citation: Obergfell K, Seifert H. 2015. Mobile DNA in the Pathogenic , p 451-469. In Craig N, Chandler M, Gellert M, Lambowitz A, Rice P, Sandmeyer S (ed), Mobile DNA III. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.MDNA3-0015-2014

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Type IV Secretion Systems
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Figures

Image of Figure 1
Figure 1

Type IV pilus and DNA uptake. (A) Type IV pilus—the Tfp is a several micron long, 60 Å wide fiber anchored in the inner membrane by PilG that extends through the PilQ secretin pore. Composed mainly of the major pilin PilE (pilin), which is processed by a dedicated protease, PilD. The PilF and PilT NTPases mediate extension and retraction of the pilus through polymerization and depolymerization of the pilin subunits. (B) Competence pseudopilus—hypothesized pseudopilus that could mediate transformation. Uses the type IV pilus complex including the PilQ pore but is not an extended fiber. Possible localization of ComP to the pseudopilus could mediate specific DNA binding. (C) DNA uptake model—retraction of the (pseudo)pilus mediated by PilT brings the initial length of DNA into the periplasm. DNA is then bound by a protein or protein complex possibly containing ComE, which mediates import of the remaining length of DNA into the periplasm. The inner membrane protein ComA facilitates DNA entry into the cytoplasm. doi:10.1128/microbiolspec.MDNA3-0015-2014.f1

Citation: Obergfell K, Seifert H. 2015. Mobile DNA in the Pathogenic , p 451-469. In Craig N, Chandler M, Gellert M, Lambowitz A, Rice P, Sandmeyer S (ed), Mobile DNA III. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.MDNA3-0015-2014
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Image of Figure 2
Figure 2

Type IV secretion system model. ParA and ParB recruit the chromosomal DNA to the type IV secretion system. TraI relaxase nicks the DNA at the site and the DNA is unwound most likely by the Yea helicase. The resulting single-stranded DNA, possibly still bound by TraI, is then secreted through the type IV secretion complex into the extracellular milieu in a contact-independent manner. The inner membrane complex is predicted to consist of TraG, TraD, and TraC with TraB spanning both the inner and outer membranes to form a channel for the DNA. The transglycosylases AtlA and LtgX create localized breaks in the peptidoglycan to allow the system to assemble. The outer membrane complex consists of TraB, TraK, and TraV. doi:10.1128/microbiolspec.MDNA3-0015-2014.f2

Citation: Obergfell K, Seifert H. 2015. Mobile DNA in the Pathogenic , p 451-469. In Craig N, Chandler M, Gellert M, Lambowitz A, Rice P, Sandmeyer S (ed), Mobile DNA III. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.MDNA3-0015-2014
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Image of Figure 3
Figure 3

Molecular description of antigenic variation. The and loci have regions of sequence microhomology (grey) and variability (colored). Sequence from a nonexpressed loci copy is transferred into the expression locus with the sequence not changing. Recombination can occur (A) in just a section of the gene resulting in a hybrid, (B) across the entire gene resulting in an entirely new variable region of , or (C) multiple times with different silent copies resulting in a new sequence containing information from different silent copies throughout the variable regions. doi:10.1128/microbiolspec.MDNA3-0015-2014.f3

Citation: Obergfell K, Seifert H. 2015. Mobile DNA in the Pathogenic , p 451-469. In Craig N, Chandler M, Gellert M, Lambowitz A, Rice P, Sandmeyer S (ed), Mobile DNA III. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.MDNA3-0015-2014
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Image of Figure 4
Figure 4

The guanine quartet (G4). (A) Gene map showing the location of the -associated G4-forming sequence and the sRNA promoter required for antigenic variation at the locus. (B) The sequence upstream of that forms a G4. Mutation of the boxed guanine residues leads to loss of antigenic variation implicating the G4 in antigenic variation. (C) The parallel G4 structure of the G4 as solved by nuclear magnetic resonance analysis. doi:10.1128/microbiolspec.MDNA3-0015-2014.f4

Citation: Obergfell K, Seifert H. 2015. Mobile DNA in the Pathogenic , p 451-469. In Craig N, Chandler M, Gellert M, Lambowitz A, Rice P, Sandmeyer S (ed), Mobile DNA III. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.MDNA3-0015-2014
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Figure 5

Proposed recombination pathways. (A) Unequal crossing-over model—a dsDNA break occurs at the locus and (I) the 5′ ends are resected by RecBCD to leave 3′ overhangs. (II) A single 3′ end mediated by RecA, invades the locus forming a D-loop. (III) The 3′ ends are extended by DNA polymerase using the gene as a template. (IV) Resolution of the double Holliday junctions results in a new sequence without altering the donor sequence. (B) Successive half crossing-over model–recombination begins with a dsDNA break or single-stranded gap in in a region of homology. (I) An RecA and RecOR mediated half crossing-over event occurs linking the and a locus on a sister chromosome. (II) A second half crossing-over event occurs in another region of microhomology downstream of the first event between the hyrbid and the original locus. (III) This recombination event leads to a new sequence at the locus and destruction of the donor chromosome. (C) Hybrid intermediate model—similar to the half crossing-over model, recombination initiates with a double-stranded break or single-stranded gap at and (I) a half crossing-over event with a donor on the same chromosome. (II) This results in a hybrid intermediate and the loss of the donor chromosome. (III) The hybrid intermediate then undergoes two recombination events with the recipient on a different chromosome. The first recombination event would occur in the extensive region of homology upstream of the genes while the second even would use microhomology within the variable regions of the genes. (IV) Resolution of the Holliday junction intermediates leads to a new sequence on the recipient chromosome. doi:10.1128/microbiolspec.MDNA3-0015-2014.f5

Citation: Obergfell K, Seifert H. 2015. Mobile DNA in the Pathogenic , p 451-469. In Craig N, Chandler M, Gellert M, Lambowitz A, Rice P, Sandmeyer S (ed), Mobile DNA III. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.MDNA3-0015-2014
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Image of Figure 6
Figure 6

Proposed antigenic variation initiation pathway. Transcription initiation at the sRNA upstream of melts the DNA allowing the G4 structure to form. An unknown protein likely binds the G4 to stabilize the structure. A single-stranded nick may occur on the strand opposite the G4 due to a stalled replication fork. RecQ could unwind the G4 structure. RecJ resects the 5′ nicked end allowing RecA to mediate recombination, possibly enhanced by binding the G4 structure, with RecOR using regions of homology between and the donor , presumably through a recombination mechanism detailed in Fig. 5 . RecG and RuvABC then process and resolve the recombination intermediate. doi:10.1128/microbiolspec.MDNA3-0015-2014.f6

Citation: Obergfell K, Seifert H. 2015. Mobile DNA in the Pathogenic , p 451-469. In Craig N, Chandler M, Gellert M, Lambowitz A, Rice P, Sandmeyer S (ed), Mobile DNA III. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.MDNA3-0015-2014
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References

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