ArticleHuman molecular genetics2013
Bardet-Biedl syndrome proteins control the cilia length through regulation of actin polymerization.
Article in Human molecular genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
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Who cites it
80 citing papers in PubMed, 116 citations in OpenAlex.
- Extracellular stressors change BBSome expression of benign mesothelial and primary pleural mesothelioma cells and affect cell adhesion and migration.Physiological reports · 2026Article
- BBSome: An essential component of hypothalamic regulation of energy homeostasis.Reviews in endocrine & metabolic disorders · 2026Review
- MENDELSEEK: An algorithm that predicts mendelian genes and elucidates what makes them special.PLoS computational biology · 2026Article
- The intraflagellar transport cycle.Nature reviews. Molecular cell biology · 2025Review
- Ciliary and Non-Ciliary Roles of IFT88 in Development and Diseases.International journal of molecular sciences · 2025Review
- BBSome deficiency in Lotmaria passim reveals divergent functions in trypanosomatid parasites.Parasites & vectors · 2025Article
- The BBS/CCT chaperonin complex ensures the localization of the adhesion G protein-coupled receptor ADGRV1 to the base of primary cilia.Frontiers in cell and developmental biology · 2025Article
- The CPLANE protein Fuzzy regulates ciliogenesis by suppressing actin polymerization at the base of the primary cilium via p190A RhoGAP.Development (Cambridge, England) · 2024Article
- Alteration of actin cytoskeletal organisation in fetal akinesia deformation sequence.Scientific reports · 2024Article
- De-Suppression of Mesenchymal Cell Identities and Variable Phenotypic Outcomes Associated with Knockout ofCells · 2023Article
- The actin-bundling protein Fascin-1 modulates ciliary signalling.Journal of molecular cell biology · 2023Article
- Organization, functions, and mechanisms of the BBSome in development, ciliopathies, and beyond.eLife · 2023Review
- Regulation of Primary Cilium Length by O-GlcNAc during Neuronal Development in a Human Neuron Model.Cells · 2023Article
- WGS Revealed NovelInternational journal of molecular sciences · 2023Article
- Modelling renal defects in Bardet-Biedl syndrome patients using human iPS cells.Frontiers in cell and developmental biology · 2023Article
- Primary cilia and actin regulatory pathways in renal ciliopathies.Frontiers in nephrology · 2023Review
- Neuronal primary cilia integrate peripheral signals with metabolic drives.Frontiers in physiology · 2023Review
- Hippocampals neurogenesis is impaired in mice with a deletion in the coiled coil domain of Talpid3-implications for Joubert syndrome.Human molecular genetics · 2022Article
- Removal of cellular protrusions.Seminars in cell & developmental biology · 2022Review
- Roles of the actin cytoskeleton in ciliogenesis.Journal of cell science · 2022Review
20 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Primary cilia are cellular appendages important for signal transduction and sensing the environment. Bardet-Biedl syndrome proteins form a complex that is important for several cytoskeleton-related processes such as ciliogenesis, cell migration and division. However, the mechanisms by which BBS proteins may regulate the cytoskeleton remain unclear. We discovered that Bbs4- and Bbs6-deficient renal medullary cells display a characteristic behaviour comprising poor migration, adhesion and division with an inability to form lamellipodial and filopodial extensions. Moreover, fewer mutant cells were ciliated [48% ± 6 for wild-type (WT) cells versus 23% ± 7 for Bbs4 null cells; P < 0.0001] and their cilia were shorter (2.55 μm ± 0.41 for WT cells versus 2.16 μm ± 0.23 for Bbs4 null cells; P < 0.0001). While the microtubular cytoskeleton and cortical actin were intact, actin stress fibre formation was severely disrupted, forming abnormal apical stress fibre aggregates. Furthermore, we observed over-abundant focal adhesions (FAs) in Bbs4-, Bbs6- and Bbs8-deficient cells. In view of these findings and the role of RhoA in regulation of actin filament polymerization, we showed that RhoA-GTP levels were highly upregulated in the absence of Bbs proteins. Upon treatment of Bbs4-deficient cells with chemical inhibitors of RhoA, we were able to restore the cilia length and number as well as the integrity of the actin cytoskeleton. Together these findings indicate that Bbs proteins play a central role in the regulation of the actin cytoskeleton and control the cilia length through alteration of RhoA levels.
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