ArticleCilia2012
Paramecium BBS genes are key to presence of channels in Cilia.
Article in Cilia, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 60 citations in OpenAlex.
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- BBSome deficiency in Lotmaria passim reveals divergent functions in trypanosomatid parasites.Parasites & vectors · 2025Article
- Identification and bioinformatics analysis of cilia-associated gene families inFrontiers in microbiology · 2025Article
- RABL2 promotes the outward transition zone passage of signaling proteins in cilia via ARL3.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- RNA interference reveals the escape response mechanism ofBiophysics and physicobiology · 2023Article
- A Review for the Special Issue onMicroorganisms · 2023Review
- An electrophysiological and kinematic model of Paramecium, the "swimming neuron".PLoS computational biology · 2023Article
- Retinal Degeneration Animal Models in Bardet-Biedl Syndrome and Related Ciliopathies.Cold Spring Harbor perspectives in medicine · 2023Review
- Cargo adapters expand the transport range of intraflagellar transport.Journal of cell science · 2022Review
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- UsingGenes · 2021Review
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- Ciliary Ca2+ pumps regulate intraciliary Ca2+ from the action potential and may co-localize with ciliary voltage-gated Ca2+ channels.The Journal of experimental biology · 2021Article
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- The role of motile cilia in the development and physiology of the nervous system.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2020Review
- Intraflagellar transport protein RABL5/IFT22 recruits the BBSome to the basal body through the GTPase ARL6/BBS3.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- A Novel Role for Polycystin-2 (Pkd2) inGenes · 2019Article
- SF-Assemblin genes inCilia · 2019Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
unlabelled
backgroundChanges in genes coding for ciliary proteins contribute to complex human syndromes called ciliopathies, such as Bardet-Biedl Syndrome (BBS). We used the model organism Paramecium to focus on ciliary ion channels that affect the beat form and sensory function of motile cilia and evaluate the effects of perturbing BBS proteins on these channels.
methodsWe used immunoprecipitations and mass spectrometry to explore whether Paramecium proteins interact as in mammalian cells. We used RNA interference (RNAi) and swimming behavior assays to examine the effects of BBS depletion on ciliary ion channels that control ciliary beating. Combining RNA interference and epitope tagging, we examined the effects of BBS depletion of BBS 7, 8 and 9 on the location of three channels and a chemoreceptor in cilia.
resultsWe found 10 orthologs of 8 BBS genes in P. tetraurelia. BBS1, 2, 4, 5, 7, 8 and 9 co-immunoprecipitate. While RNAi reduction of BBS 7 and 9 gene products caused loss and shortening of cilia, RNAi for all BBS genes except BBS2 affected patterns of ciliary motility that are governed by ciliary ion channels. Swimming behavior assays pointed to loss of ciliary K+ channel function. Combining RNAi and epitope tagged ciliary proteins we demonstrated that a calcium activated K+ channel was no longer located in the cilia upon depletion of BBS 7, 8 or 9, consistent with the cells' swimming behavior. The TRPP channel PKD2 was also lost from the cilia. In contrast, the ciliary voltage gated calcium channel was unaffected by BBS depletion, consistent with behavioral assays. The ciliary location of a chemoreceptor for folate was similarly unperturbed by the depletion of BBS 7, 8 or 9.
conclusionsThe co-immunoprecipitation of BBS 1,2,4,5,7,8, and 9 suggests a complex of BBS proteins. RNAi for BBS 7, 8 or 9 gene products causes the selective loss of K+ and PKD2 channels from the cilia while the critical voltage gated calcium channel and a peripheral receptor protein remain undisturbed. These channels govern ciliary beating and sensory function. Importantly, in P. tetraurelia we can combine studies of ciliopathy protein function with behavior and location and control of ciliary channels.
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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.