ArticleJournal of bacteriology2010
Genomic island 2 is an unstable genetic element contributing to Brucella lipopolysaccharide spontaneous smooth-to-rough dissociation.
Article in Journal of bacteriology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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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.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- A critical review of diagnostic methods for camel brucellosis.Veterinary and animal science · 2026Review
- Investigation of genomic island 2 deciphers the evolution of a genus Brucella.Scientific reports · 2025Article
- Brucellosis: Unveiling the complexities of a pervasive zoonotic disease and its global impacts.Open veterinary journal · 2024Review
- Article
- Genomic Island-Mediated Horizontal Transfer of the Erythromycin Resistance GeneApplied and environmental microbiology · 2022Article
- Facing the Human and Animal Brucellosis Conundrums: The Forgotten Lessons.Microorganisms · 2022Article
- When the Going Gets Rough: The Significance ofFrontiers in microbiology · 2021Review
- Localized incorporation of outer membrane components in the pathogenThe EMBO journal · 2019Article
- Structural Studies of Lipopolysaccharide-defective Mutants from Brucella melitensis Identify a Core Oligosaccharide Critical in Virulence.The Journal of biological chemistry · 2016Article
- Brucella canis is an intracellular pathogen that induces a lower proinflammatory response than smooth zoonotic counterparts.Infection and immunity · 2015Article
- Smooth to Rough Dissociation in Brucella: The Missing Link to Virulence.Frontiers in cellular and infection microbiology · 2015Article
- Brucella dissociation is essential for macrophage egress and bacterial dissemination.Frontiers in cellular and infection microbiology · 2014Article
- Deletion of the GI-2 integrase and the wbkA flanking transposase improves the stability of Brucella melitensis Rev 1 vaccine.Veterinary research · 2013Article
- Diverse genetic regulon of the virulence-associated transcriptional regulator MucR in Brucella abortus 2308.Infection and immunity · 2013Article
- What have we learned from brucellosis in the mouse model?Veterinary research · 2012Review
- Spontaneous excision of the O-polysaccharide wbkA glycosyltranferase gene is a cause of dissociation of smooth to rough Brucella colonies.Journal of bacteriology · 2012Article
- Lipopolysaccharide-Deficient Brucella Variants Arise Spontaneously during Infection.Frontiers in microbiology · 2011Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Brucella is a Gram-negative bacterium that causes a worldwide-distributed zoonosis. The genus includes smooth (S) and rough (R) species that differ in the presence or absence, respectively, of the O-polysaccharide of lipopolysaccharide. In S brucellae, the O-polysaccharide is a critical diagnostic antigen and a virulence determinant. However, S brucellae spontaneously dissociate into R forms, a problem in antigen and S vaccine production. Spontaneous R mutants of Brucella abortus, Brucella melitensis, and Brucella suis carried the chromosomal scar corresponding to genomic island 2 (GI-2) excision, an event causing the loss of the wboA and wboB O-polysaccharide genes, and the predicted excised circular intermediate was identified in B. abortus, B. melitensis, and B. suis cultures. Moreover, disruption of a putative phage integrase gene in B. abortus GI-2 caused a reduction in O-polysaccharide loss rates under conditions promoting S-R dissociation. However, spontaneous R mutants not carrying the GI-2 scar were also detected. These results demonstrate that the phage integrase-related GI-2 excision is a cause of S-R brucella dissociation and that other undescribed mechanisms must also be involved. In the R Brucella species, previous works have shown that Brucella ovis but not Brucella canis lacks GI-2, and a chromosomal scar identical to those in R mutants was observed. These results suggest that the phage integrase-promoted GI-2 excision played a role in B. ovis speciation and are consistent with other evidence, suggesting that this species and B. canis have emerged as two independent lineages.
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Registered trials
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.