XerCD-Mediated Site-Specific Recombination Leads to Loss of the 57-Kilobase Gonococcal Genetic Island

Domínguez, Nadia M.; Hackett, Kathleen T.; Dillard, Joseph P.

doi:10.1128/jb.00948-10

Cited by 41 publications

(62 citation statements)

References 41 publications

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“…IMEXs are nevertheless rarely excised and lost. The GGI is present in 80% of N. gonorrheae strains and the excised form is barely detected (8,9). We have shown here that the integrated form of the GGI is flanked by two active Xer sites.…”

Section: Discussionmentioning

confidence: 68%

“…Comparison of N. gonorrheae strains harboring or lacking the GGI, together with functional data, indicates that the GGI integrates by XerCD-dependent recombination (9). The nonreplicative excised circular form of the GGI can be detected and the GGI can also be lost, showing that excision occurs, although at low frequencies (9). Although the GGI…”

mentioning

confidence: 97%

“…How IMEXs integrate into dif without inactivating its cellular function and how they are stably maintained in their integrated state has remained unclear despite study over the past decade (4-7). Here we answer these questions by studying the gonococcal genomic island (GGI), an IMEX stably integrated into the dif site of pathogenic Neisseria species that encodes crucial functions for gene exchange and virulence (8,9).…”

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confidence: 99%

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FtsK translocation permits discrimination between an endogenous and an imported Xer/ dif recombination complex

Fournes

Crozat

Pages

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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In bacteria, the FtsK/Xer/dif (chromosome dimer resolution site) system is essential for faithful vertical genetic transmission, ensuring the resolution of chromosome dimers during their segregation to daughter cells. This system is also targeted by mobile genetic elements that integrate into chromosomal dif sites. A central question is thus how Xer/dif recombination is tuned to both act in chromosome segregation and stably maintain mobile elements. To explore this question, we focused on pathogenic Neisseria species harboring a genomic island in their dif sites. We show that the FtsK DNA translocase acts differentially at the recombination sites flanking the genomic island. It stops at one Xer/dif complex, activating recombination, but it does not stop on the other site, thus dismantling it. FtsK translocation thus permits cis discrimination between an endogenous and an imported Xer/dif recombination complex.

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Section: Discussionmentioning

confidence: 68%

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confidence: 97%

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confidence: 99%

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FtsK translocation permits discrimination between an endogenous and an imported Xer/ dif recombination complex

Fournes

Crozat

Pages

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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“…The secreted DNA also acts in the initiation of biofilm development (5). The genes for the gonococcal T4SS are encoded on the gonococcal genetic island (GGI), a 57-kb genetic island that was likely horizontally acquired and is inserted in the chromosome near the replication terminus (1,2,6). T4SSs are a diverse family of transmembrane complexes that include both conjugation systems (such as F plasmid and the IncN plasmid pKM101) and effector translocator systems that deliver proteins or DNAprotein complexes directly into host cells (such as the well-studied VirB/D T4SS in Agrobacterium tumefaciens) (7)(8)(9)(10).…”

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confidence: 99%

TraK and TraB Are Conserved Outer Membrane Proteins of the Neisseria gonorrhoeae Type IV Secretion System and Are Expressed at Low Levels in Wild-Type Cells

et al. 2014

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b Neisseria gonorrhoeae uses a type IV secretion system (T4SS) to secrete chromosomal DNA into the medium, and this DNA is effective in transforming other gonococci via natural transformation. In addition, the T4SS is important in the initial stages of biofilm development and mediates intracellular iron uptake in the absence of TonB. To better understand the mechanism of type IV secretion in N. gonorrhoeae, we examined the expression levels and localization of two predicted T4SS outer membrane proteins, TraK and TraB, in the wild-type strain as well as in overexpression strains and in a strain lacking all of the T4SS proteins. Despite very low sequence similarity to known homologues, TraB (VirB10 homolog) and TraK (VirB9 homolog) localized similarly to related proteins in other systems. Additionally, we found that TraV (a VirB7 homolog) interacts with TraK, as in other T4SSs. However, unlike in other systems, neither TraK nor TraB required the presence of other T4SS components for proper localization. Unlike other gonococcal T4SS proteins we have investigated, protein levels of the outer membrane proteins TraK and TraB were extremely low in wild-type cells and were undetectable by Western blotting unless overexpressed or tagged with a FLAG3 triple-epitope tag. Localization of TraK-FLAG3 in otherwise wild-type cells using immunogold electron microscopy of thin sections revealed a single gold particle on some cells. These results suggest that the gonococcal T4SS may be present in single copy per cell and that small amounts of T4SS proteins TraK and TraB are sufficient for DNA secretion.

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“…It was previously suggested that GGI initially harbored true neisserial dif sites and that their stabilization resulted from mutations that occurred after their integration (5). Many different types of mutations, including mutations in the central region of the dif sites and mutations abolishing the binding of the recombinases to them, could impede Xer recombination.…”

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confidence: 99%

How Xer-exploiting mobile elements overcome cellular control

Midonet¹,

Barre²

2016

Proc. Natl. Acad. Sci. U.S.A.

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International audienceMost strains of Neisseria gonorrheae (Ng), the causative agent of the sexually transmitted disease gonorrheae, and a few strains of Neisseria meningitidis (Nm), which is responsible for a large number of meningitides, harbor a 57-kb horizontally acquired genetic element, the gonococcal genomic island (GGI) (1⇓–3). Certain versions of the GGI are associated with disseminated gonococcal infection (1, 4). In addition, the GGI encodes numerous homologs of type IV secretion system genes, which are necessary for DNA secretion and facilitate natural transformation of the Neisseria (1, 2, 4). GGI are found integrated at the chromosomal dimer resolution site of their host chromosome, dif, and are flanked by a partial repeat of it, difGGI (Fig. 1A) (1, 5). The dif site is the target of two highly conserved chromosomally encoded tyrosine recombinases, XerC and XerD, which normally serve to resolve dimers of circular chromosomes through the addition of a crossover between directly repeated dif sites (6). This reaction raises questions on how GGI could be stably maintained (5). The results presented by Fournes et al. (7) in PNAS shed a new light on this apparent paradox

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XerCD-Mediated Site-Specific Recombination Leads to Loss of the 57-Kilobase Gonococcal Genetic Island

Cited by 41 publications

References 41 publications

FtsK translocation permits discrimination between an endogenous and an imported Xer/ dif recombination complex

FtsK translocation permits discrimination between an endogenous and an imported Xer/ dif recombination complex

TraK and TraB Are Conserved Outer Membrane Proteins of the Neisseria gonorrhoeae Type IV Secretion System and Are Expressed at Low Levels in Wild-Type Cells

How Xer-exploiting mobile elements overcome cellular control

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