Evidence map›Paper›PMID 21075927›Full record

ArticleJournal of bacteriology2011

XerCD-mediated site-specific recombination leads to loss of the 57-kilobase gonococcal genetic island.

Nadia M Domínguez, Kathleen T Hackett, Joseph P Dillard

Open access · greenAbstract read
In one paragraph

Article in Journal of bacteriology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.2field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed, 44 citations in OpenAlex.

  1. A small RNA fromVirulence · 2025
    Article
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  13. Review
  14. How Xer-exploiting mobile elements overcome cellular control.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  15. FtsK translocation permits discrimination between an endogenous and an imported Xer/dif recombination complex.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Mobile DNA in the pathogenicMicrobiology spectrum · 2015
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Nadia M DomínguezDepartment of Medical Microbiology and Immunology, University of Wisconsin--Madison School of Medicine and Public Health, Madison, WI 53706, USA.
Kathleen T Hackett
Joseph P Dillard
University of Wisconsin–Madison · US

Funding

BIOTECHNOLOGY TRAINING PROGRAMT32GM008349 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI FOX, BRIAN G · 1989 to 2019
$22.5M
Type IV Secretion by Neisseria gonorrhoeaeR01AI047958 · NIAID · UNIVERSITY OF WISCONSIN-MADISON · PI DILLARD, JOSEPH P · 2002 to 2019
$5.0M
Gain and loss of the gonococcal genetic island in NeisseriaR21AI072605 · NIAID · UNIVERSITY OF WISCONSIN-MADISON · PI DILLARD, JOSEPH P · 2007 to 2008
$392k
NIAID NIH HHS AI047958NIAID NIH HHS AI072605NIAID NIH HHS R01 AI047958NIAID NIH HHS R21 AI072605NIGMS NIH HHS 5 T32 GM008349NIGMS NIH HHS T32 GM008349
6 · The paper itself

Abstract

Most strains of Neisseria gonorrhoeae carry the 57-kb gonococcal genetic island (GGI), as do a few strains of Neisseria meningitidis. The GGI is inserted into the chromosome at the dif site (difA) and is flanked by a partial repeat of the dif site (difB). Since dif is a sequence recognized by the site-specific recombinases XerC and XerD and the GGI shows evidence of horizontal acquisition, we hypothesized that the GGI may be acquired or lost by XerCD-mediated site-specific recombination. We show that while the GGI flanked by wild-type dif sites, difA and difB, is not readily lost from the gonococcal chromosome, the substitution of difB with another copy of difA allows the frequent excision and loss of the GGI. In mutants carrying two difA sites (difA(+) difA(+)), the GGI can be detected as an extrachromosomal circle that exists transiently. A mutation of xerD diminished GGI excision from the chromosome of a difA(+) difA(+) strain, while mutations in recA or type IV secretion genes had no effect on the loss of the GGI. These data indicate that the GGI is maintained by the replication of the chromosome and that GGI excision and loss are dependent upon the dif sequence and xerD. The detection of a circular form of the GGI in a wild-type strain suggests that GGI excision may occur naturally and could function to facilitate GGI transfer. These data suggest a model of GGI excision and loss explaining the absence of the GGI from some gonococcal strains and the maintenance of variant GGIs in some gonococcal and meningococcal isolates.

Indexed as

Genomic IslandsRecombination, GeneticSequence DeletionBacterial ProteinsIntegrasesModels, BiologicalMutationNeisseria gonorrhoeaeRecombinasesBacterial ProteinsIntegrasesRecombinases

Identifiers

PMID21075927
PMCPMC3019826
OpenAlexW2148799912

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.