ArticleProceedings of the National Academy of Sciences of the United States of America2005
Brucella coopts the small GTPase Sar1 for intracellular replication.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.
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Who cites it
88 citing papers in PubMed, 164 citations in OpenAlex.
- Pathogenesis of Brucella abortus and Brucella melitensis in bovine and ovine-derived trophoblasts and macrophages and impaired intracellular trafficking of the Rev1 vaccine strain.Veterinary research · 2026Article
- Brucellosis: Bacteriology, pathogenesis, epidemiology and role of the metallophores in virulence: a review.Frontiers in cellular and infection microbiology · 2025Review
- The battle between bacterial infection and autophagy in aquatic animals.Frontiers in immunology · 2025Review
- The putative type 4 secretion system effector BspD is involved in maintaining envelope integrity of the pathogenmSphere · 2024Article
- A genome-wide CRISPR screen identified host genes essential for intracellularMicrobiology spectrum · 2024Article
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- Host cell egress of Brucella abortus requires BNIP3L-mediated mitophagy.The EMBO journal · 2023Article
- The Brucella abortus Type IV Effector BspA Inhibits MARCH6-Dependent ERAD To Promote Intracellular Growth.Infection and immunity · 2023Article
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- The mechanism of chronic intracellular infection withFrontiers in cellular and infection microbiology · 2023Review
- The endoplasmic reticulum stress-mediated unfolded protein response protects against infection of goat endometrial epithelial cells byVirulence · 2022Article
- Antibiotic persistence of intracellular Brucella abortus.PLoS neglected tropical diseases · 2022Article
- 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
- Article
- Intracellular Passage Triggers a Molecular Response in Brucella abortus That Increases Its Infectiousness.Infection and immunity · 2021Article
- Integrative Bioinformatics Indentification of the Autophagic Pathway-Associated miRNA-mRNA Networks in RAW264.7 Macrophage Cells Infected with ∆Omp25 Brucella melitensis.Inflammation · 2020Article
- Epistatic Interplay between Type IV Secretion Effectors Engages the Small GTPase Rab2 in themBio · 2020Article
- A Role for the VPS Retromer inmSphere · 2019Article
28 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathogen Brucella abortus resides inside macrophages within a unique, replication-permissive organelle that is derived from the endoplasmic reticulum (ER). Although dependent on the Brucella type IV secretion system VirB, the mechanisms governing the biogenesis of this compartment remain elusive. Here, we investigated a putative role of the early secretory pathway in ER membrane accretion by the Brucella-containing vacuoles (BCVs). We show that BCVs interact with ER exit sites (ERES), and blockade of Sar1 activity, which disrupts ERES, prevents intracellular replication of Brucella. In cells expressing the dominant interfering form Sar1[T39N], BCVs do not acquire ER membranes, suggesting that they are unable to mature into replicative organelles. By contrast, treatments that block subsequent secretory events do not affect bacterial replication. We propose that Sar1-dependent ERES functions, but not subsequent secretory events, are essential for the biogenesis of the Brucella replicative compartment and, thus, bacterial replication. These results assign an essential role for Sar1 in pathogenesis of an intracellular bacterium.
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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.