ArticlePLoS biology2024
Cep131-Cep162 and Cby-Fam92 complexes cooperatively maintain Cep290 at the basal body and contribute to ciliogenesis initiation.
Article in PLoS biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Article
- Ciliopathy-related B9 protein complex regulates ciliary axonemal microtubule posttranslational modifications and initiation of ciliogenesis.The Journal of clinical investigation · 2026Article
- CCHCR1 links P-body proteins to the centrosome and is required for ciliogenesis through interacting with OFD1 and PCM1.Cellular & molecular biology letters · 2025Article
- The Kinesin Motor Kif9 Disrupts Primary Cilia Length by Mispositioning Centriolar Satellites.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- CEP162: A critical regulator of ciliary transition zone assembly and its implications in ciliopathies.Journal of cell communication and signaling · 2025Review
- Synchronized temporal-spatial analysis via microscopy and phosphoproteomics (STAMP) of quiescence.Science advances · 2025Article
- Article
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11 authors at 4 institutions in 2 countries.
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Abstract
Cilia play critical roles in cell signal transduction and organ development. Defects in cilia function result in a variety of genetic disorders. Cep290 is an evolutionarily conserved ciliopathy protein that bridges the ciliary membrane and axoneme at the basal body (BB) and plays critical roles in the initiation of ciliogenesis and TZ assembly. How Cep290 is maintained at BB and whether axonemal and ciliary membrane localized cues converge to determine the localization of Cep290 remain unknown. Here, we report that the Cep131-Cep162 module near the axoneme and the Cby-Fam92 module close to the membrane synergistically control the BB localization of Cep290 and the subsequent initiation of ciliogenesis in Drosophila. Concurrent deletion of any protein of the Cep131-Cep162 module and of the Cby-Fam92 module leads to a complete loss of Cep290 from BB and blocks ciliogenesis at its initiation stage. Our results reveal that the first step of ciliogenesis strictly depends on cooperative and retroactive interactions between Cep131-Cep162, Cby-Fam92 and Cep290, which may contribute to the complex pathogenesis of Cep290-related ciliopathies.
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