ArticlePloS one2018
BBS1 is involved in retrograde trafficking of ciliary GPCRs in the context of the BBSome complex.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 66 citations in OpenAlex.
- Intraflagellar transport-20 guides the ciliary membrane trafficking of channelrhodopsin in Chlamydomonas reinhardtii.Molecular biology reports · 2026Article
- Bardet-Biedl syndrome 1 mutations differentially impact BBSome integrity and ciliary trafficking.Cell communication and signaling : CCS · 2026Article
- BBSome: An essential component of hypothalamic regulation of energy homeostasis.Reviews in endocrine & metabolic disorders · 2026Review
- Homology search confirms widespread presence of BBSome proteins in Hexapoda with implications for potential non-ciliary BBS protein functions in honey bees.Scientific reports · 2025Article
- Mutually independent and cilia-independent assembly of IFT-A and IFT-B complexes at mother centriole.Molecular biology of the cell · 2025Article
- Linkage between Fuz and Gpr161 genes regulates sonic hedgehog signaling during mouse neural tube development.Development (Cambridge, England) · 2024Article
- Joubert syndrome causing mutation in C2 domain of CC2D2A affects structural integrity of cilia and cellular signaling molecules.Experimental brain research · 2024Article
- The novel linkage betweenbioRxiv : the preprint server for biology · 2024Article
- De-Suppression of Mesenchymal Cell Identities and Variable Phenotypic Outcomes Associated with Knockout ofCells · 2023Article
- Organization, functions, and mechanisms of the BBSome in development, ciliopathies, and beyond.eLife · 2023Review
- Biallelic Variants in Seven Different Genes Associated with Clinically Suspected Bardet-Biedl Syndrome.Genes · 2023Article
- Multiple interactions of the dynein-2 complex with the IFT-B complex are required for effective intraflagellar transport.Journal of cell science · 2023Article
- Cellular and Molecular Mechanisms of Pathogenesis Underlying Inherited Retinal Dystrophies.Biomolecules · 2023Review
- Modelling renal defects in Bardet-Biedl syndrome patients using human iPS cells.Frontiers in cell and developmental biology · 2023Article
- Recent advances in the understanding of cilia mechanisms and their applications as therapeutic targets.Frontiers in molecular biosciences · 2023Review
- Article
- CEP19-RABL2-IFT-B axis controls BBSome-mediated ciliary GPCR export.Molecular biology of the cell · 2022Article
- BROMI/TBC1D32 together with CCRK/CDK20 and FAM149B1/JBTS36 contributes to intraflagellar transport turnaround involving ICK/CILK1.Molecular biology of the cell · 2022Article
- Ciliary signaling proteins are mislocalized in the brains of Bardet-Biedl syndrome 1-null mice.Frontiers in cell and developmental biology · 2022Article
- Neuronal cilia in energy homeostasis.Frontiers in cell and developmental biology · 2022Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Protein trafficking within cilia is mediated by the intraflagellar transport (IFT) machinery composed of large protein complexes. The BBSome consists of eight BBS proteins encoded by causative genes of Bardet-Biedl syndrome (BBS), and has been implicated in the trafficking of ciliary membrane proteins, including G protein-coupled receptors (GPCRs), by connecting the IFT machinery to cargo GPCRs. Membrane recruitment of the BBSome to promote cargo trafficking has been proposed to be regulated by the Arf-like small GTPase ARL6/BBS3, through its interaction with the BBS1 subunit of the BBSome. We here investigated how the BBSome core subcomplex composed of BBS1, BBS2, BBS7, and BBS9 assembles and interacts with ARL6, and found that the ARL6-BBS1 interaction is reinforced by BBS9. BBS1-knockout (KO) cells showed defects in the ciliary entry of other BBSome subunits and ARL6, and in ciliary retrograde trafficking and the export of the GPCRs, Smoothened and GPR161. The trafficking defect of these GPCRs was rescued by the exogenous expression of wild-type BBS1, but not by its mutant lacking BBS9-binding ability. Our data thus indicate that the intact BBSome is required for retrograde trafficking of GPCRs out of cilia.
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