ArticleMolecular microbiology2013
The Leishmania major BBSome subunit BBS1 is essential for parasite virulence in the mammalian host.
Article in Molecular microbiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 21 citations in OpenAlex.
- Article
- BBSome deficiency in Lotmaria passim reveals divergent functions in trypanosomatid parasites.Parasites & vectors · 2025Article
- From classical approaches to new developments in genetic engineering of live attenuated vaccine against cutaneous leishmaniasis: potential and immunization.Frontiers in public health · 2024Review
- Next-Generation Leishmanization: Revisiting Molecular Targets for Selecting Genetically Engineered Live-AttenuatedMicroorganisms · 2023Review
- Challenges and Tools for In VitroPathogens (Basel, Switzerland) · 2021Review
- Global genome diversity of theeLife · 2020Article
- Nanoparticle-mediated magnetic hyperthermia is an effective method for killing the human-infective protozoan parasite Leishmania mexicana in vitro.Scientific reports · 2019Article
- Trafficking of ciliary membrane proteins by the intraflagellar transport/BBSome machinery.Essays in biochemistry · 2018Review
- Development of Trypanosoma cruzi in vitro assays to identify compounds suitable for progression in Chagas' disease drug discovery.PLoS neglected tropical diseases · 2018Article
- Development of NanoLuc-PEST expressing Leishmania mexicana as a new drug discovery tool for axenic- and intramacrophage-based assays.PLoS neglected tropical diseases · 2018Article
- The molecular machines that traffic signaling receptors into and out of cilia.Current opinion in cell biology · 2018Review
- Cutaneous leishmaniasis in northwestern Saudi Arabia: identification of sand fly fauna and parasites.Parasites & vectors · 2017Article
- Loss of the BBSome perturbs endocytic trafficking and disrupts virulence of Trypanosoma brucei.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Global analysis of protein N-myristoylation and exploration of N-myristoyltransferase as a drug target in the neglected human pathogen Leishmania donovani.Chemistry & biology · 2015Article
- Kharon1 null mutants of Leishmania mexicana are avirulent in mice and exhibit a cytokinesis defect within macrophages.PloS one · 2015Article
- Transcriptional profiling of the spleen in progressive visceral leishmaniasis reveals mixed expression of type 1 and type 2 cytokine-responsive genes.BMC immunology · 2014Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Bardet-Biedl syndrome (BBS) is a human genetic disorder with a spectrum of symptoms caused by primary cilium dysfunction. The disease is caused by mutations in one of at least 17 identified genes, of which seven encode subunits of the BBSome, a protein complex required for specific trafficking events to and from the primary cilium. The molecular mechanisms associated with BBSome function remain to be fully elucidated. Here, we generated null and complemented mutants of the BBSome subunit BBS1 in the protozoan parasite, Leishmania. In the absence of BBS1, extracellular parasites have no apparent defects in growth, flagellum assembly, motility or differentiation in vitro but there is accumulation of vacuole-like structures close to the flagellar pocket. Infectivity of these parasites for macrophages in vitro is reduced compared with wild-type controls but the null parasites retain the ability to differentiate to the intracellular amastigote stage. However, infectivity of BBS1 null parasites is severely compromised in a BALB/c mouse footpad model. We hypothesize that the absence of BBS1 in Leishmania leads to defects in specific trafficking events that affect parasite persistence in the host. This is the first report of an association between the BBSome complex and pathogen infectivity.
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