ArticleCellular microbiology2014
Identification of a type IV secretion substrate of Brucella abortus that participates in the early stages of intracellular survival.
Article in Cellular microbiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed.
- Type IV secretion systems: reconciling diversity through a unified nomenclature.FEMS microbiology reviews · 2026Review
- Beyond survival to domination:Frontiers in microbiology · 2025Review
- ThemicroLife · 2025Review
- Article
- Article
- Review
- The Brucella abortus Type IV Effector BspA Inhibits MARCH6-Dependent ERAD To Promote Intracellular Growth.Infection and immunity · 2023Article
- Antibiotic persistence of intracellular Brucella abortus.PLoS neglected tropical diseases · 2022Article
- Article
- Article
- The VirB System Plays a Crucial Role inInternational journal of molecular sciences · 2021Review
- A Brucella effector modulates the Arf6-Rab8a GTPase cascade to promote intravacuolar replication.The EMBO journal · 2021Article
- Uncovering the Hidden Credentials ofMicrobiology and molecular biology reviews : MMBR · 2021Review
- Review
- Proteomics of Brucella.Proteomes · 2020Review
- Epistatic Interplay between Type IV Secretion Effectors Engages the Small GTPase Rab2 in themBio · 2020Article
- Article
- PhiA, a Peptidoglycan Hydrolase Inhibitor ofInfection and immunity · 2019Article
- The Intracellular Life Cycle ofMicrobiology spectrum · 2019Review
- MapB, the Brucella suis TamB homologue, is involved in cell envelope biogenesis, cell division and virulence.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Brucella abortus, the aetiological agent of bovine brucellosis, is an intracellular pathogen whose virulence is completely dependent on a type IV secretion system. This secretion system translocates effector proteins into the host cell to modulate the intracellular fate of the bacterium in order to establish a secure niche were it actively replicates. Although much has been done in understanding how this secretion system participates in the virulence process, few effector proteins have been identified to date. We describe here the identification of a type IV secretion substrate (SepA) that is only present in Brucella spp. and has no detectable homology to known proteins. This protein is secreted in a virB-dependent manner in a two-step process involving a periplasmic intermediate and secretion is necessary for its function. The deletion mutant showed a defect in the early stages of intracellular replication in professional and non-professional phagocytes although it invades the cells more efficiently than the wild-type parental strain. Our results indicate that, even though the mutant was more invasive, it had a defect in excluding the lysosomal marker Lamp-1 and was inactivated more efficiently during the early phases of the intracellular life cycle.
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Registered trials
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