ArticleNature communications2018
Axoneme polyglutamylation regulated by Joubert syndrome protein ARL13B controls ciliary targeting of signaling molecules.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 96 citations in OpenAlex.
- ASD mutations in the ciliary gene CEP41 impact development of projection neurons and interneurons in a human cortical organoid model.Molecular psychiatry · 2026Article
- Post-Translational Modifications of Tubulin in Oocyte Maturation and Female Infertility.Cytoskeleton (Hoboken, N.J.) · 2026Review
- Primary cilium disassembly - from mechanisms to roles in physiology and disease.Journal of cell science · 2026Review
- Insights into retinal disease and non-tubulin glutamylation from a RPGR-TTLL5 complex structure.The Journal of cell biology · 2026Article
- FLNB and TTC26 regulate ciliary Hedgehog signaling to maintain intervertebral disc matrix homeostasis in adolescent idiopathic scoliosis.Genome biology · 2026Article
- Identification of a component of the tubulin poly-glutamylase complex required for phosphoinositide homeostasis and cilium assembly and maintenance.Nature communications · 2026Article
- Tubulin glutamylation: a key regulator of flagella, cilia, centrosomes, and disease pathways.Journal of biomedical science · 2026Review
- ALIX and ITCH localize to the base of primary cilia and negatively regulate ciliary Polycystin-2 levels.BMC molecular and cell biology · 2026Article
- Ciliopathy-related B9 protein complex regulates ciliary axonemal microtubule posttranslational modifications and initiation of ciliogenesis.The Journal of clinical investigation · 2026Article
- KLC3 regulates axonemal glutamylation via RAB11/FIP5 in polycystic kidney disease.Cell communication and signaling : CCS · 2025Article
- Rescue of ciliogenesis and hyperglutamylation mutant phenotype in AGBL5BMC molecular and cell biology · 2025Article
- Targeting p-FGFR1Biomedicines · 2025Article
- CFAP100 couples microtubule glutamylation to spindle pole integrity in keratinocytes to promote epidermal development.Nature communications · 2025Article
- Variants in the AGBL5 gene are responsible for autosomal recessive Retinitis pigmentosa with hearing loss.European journal of human genetics : EJHG · 2025Article
- Non-canonical CDK6 activity promotes cilia disassembly by suppressing axoneme polyglutamylation.The Journal of cell biology · 2025Article
- The chloroplast-located HKT transporter plays an important role in fertilization and development in Physcomitrium patens.The Plant journal : for cell and molecular biology · 2025Article
- Loss of Kat2b impairs intraflagellar transport and the Hedgehog signaling pathway in primary cilia.Scientific reports · 2025Article
- Glutamylation imbalance impairs the molecular architecture of the photoreceptor cilium.The EMBO journal · 2024Article
- Structural basis for α-tubulin-specific and modification state-dependent glutamylation.Nature chemical biology · 2024Article
- Carboxy-terminal polyglutamylation regulates signaling and phase separation of the Dishevelled protein.The EMBO journal · 2024Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Tubulin polyglutamylation is a predominant axonemal post-translational modification. However, if and how axoneme polyglutamylation is essential for primary cilia and contribute to ciliopathies are unknown. Here, we report that Joubert syndrome protein ARL13B controls axoneme polyglutamylation, which is marginally required for cilia stability but essential for cilia signaling. ARL13B interacts with RAB11 effector FIP5 to promote cilia import of glutamylase TTLL5 and TTLL6. Hypoglutamylation caused by a deficient ARL13B-RAB11-FIP5 trafficking pathway shows no effect on ciliogenesis, but promotes cilia disassembly and, importantly, impairs cilia signaling by disrupting the proper anchoring of sensory receptors and trafficking of signaling molecules. Remarkably, depletion of deglutamylase CCP5, the predominant cilia deglutamylase, effectively restores hypoglutamylation-induced cilia defects. Our study reveals a paradigm that tubulin polyglutamylation is a major contributor for cilia signaling and suggests a potential therapeutic strategy by targeting polyglutamylation machinery to promote ciliary targeting of signaling machineries and correct signaling defects in ciliopathies.
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