ArticleJournal of bacteriology2008
Genomic island 2 of Brucella melitensis is a major virulence determinant: functional analyses of genomic islands.
Article in Journal of bacteriology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
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- When the Going Gets Rough: The Significance ofFrontiers in microbiology · 2021Review
- The Twin-Arginine Translocation System Is Important for Stress Resistance and Virulence of Brucella melitensis.Infection and immunity · 2020Article
- WadD, a NewFrontiers in microbiology · 2018Article
- TfoX-based genetic mapping identifies Vibrio fischeri strain-level differences and reveals a common lineage of laboratory strains.Journal of bacteriology · 2015Article
- Decreased in vivo virulence and altered gene expression by a Brucella melitensis light-sensing histidine kinase mutant.Pathogens and disease · 2015Article
- Smooth to Rough Dissociation in Brucella: The Missing Link to Virulence.Frontiers in cellular and infection microbiology · 2015Article
- Main functions and taxonomic distribution of virulence genes in Brucella melitensis 16 M.PloS one · 2014Article
- Deletion of the GI-2 integrase and the wbkA flanking transposase improves the stability of Brucella melitensis Rev 1 vaccine.Veterinary research · 2013Article
- Comparison of genomes of Brucella melitensis M28 and the B. melitensis M5-90 derivative vaccine strain highlights the translation elongation factor Tu gene tuf2 as an attenuation-related gene.Infection and immunity · 2013Article
- A lysozyme-like protein in Brucella abortus is involved in the early stages of intracellular replication.Infection and immunity · 2013Article
- Brucella induces an unfolded protein response via TcpB that supports intracellular replication in macrophages.PLoS pathogens · 2013Article
- Spontaneous excision of the O-polysaccharide wbkA glycosyltranferase gene is a cause of dissociation of smooth to rough Brucella colonies.Journal of bacteriology · 2012Article
- High-density transcriptional initiation signals underline genomic islands in bacteria.PloS one · 2012Article
- Characterization of genomic island 3 and genetic variability of Chilean field strains of Brucella abortus.Journal of clinical microbiology · 2011Article
- Genomic island 2 is an unstable genetic element contributing to Brucella lipopolysaccharide spontaneous smooth-to-rough dissociation.Journal of bacteriology · 2010Article
- Brucella melitensis, B. neotomae and B. ovis elicit common and distinctive macrophage defense transcriptional responses.Experimental biology and medicine (Maywood, N.J.) · 2009Article
- Brucella microti: the genome sequence of an emerging pathogen.BMC genomics · 2009Article
- Analysis of ten Brucella genomes reveals evidence for horizontal gene transfer despite a preferred intracellular lifestyle.Journal of bacteriology · 2009Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Brucella genomic islands (GIs) share similarities in their genomic organization to pathogenicity islands from other bacteria and are likely acquired by lateral gene transfer. Here, we report the identification of a GI that is important for the pathogenicity of Brucella melitensis. The deletion of GI-1, GI-5, or GI-6 did not affect bacterial growth in macrophages as well as their virulence in interferon regulatory factor 1-deficient (IRF-1(-/-)) mice, suggesting that these islands do not contribute to Brucella virulence. However, the deletion of GI-2 resulted in the attenuation of bacterial growth in macrophages and virulence in IRF-1(-/-) mice. The GI-2 mutant also displayed a rough lipopolysaccharide (LPS) phenotype indicated by acriflavin agglutination, suggesting that in vitro and in vivo attenuation is a result of LPS alteration. Further, systematic analysis of the entire GI-2 revealed two open reading frames (ORFs), BMEI0997 and I0998, that encode hypothetical sugar transferases and contribute to LPS alteration, as the deletion of either of these ORFs resulted in a rough phenotype similar to that of the GI-2 mutant. Complementation analyses indicated that in addition to I0997 and I0998, I0999 is required to restore the smooth LPS in the GI-2 mutant as well as its full in vitro and in vivo virulence. The I0999 sequence analysis suggested that it might function as a transporter to help facilitate the transport or linking of the O antigen to the LPS. Our study also indicated that the rough LPS resulting from the GI-2 deletion may affect pathogen-associated molecular pattern recognition by Toll-like receptors.
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