ArticleCell communication and signaling : CCS2025
Tau-tubulin kinase 2 restrains microtubule-depolymerizer KIF2A to support primary cilia growth.
Article in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Selective Brain-Penetrant TTBK1 Inhibitors Modulate TDP-43 Pathology and Rescue Cognitive Deficits in a Mouse Model of TDP-43 Proteinopathy.Journal of medicinal chemistry · 2026Article
- Primary cilia-extracellular vesicle crosstalk in Alzheimer's disease: Emerging mechanisms and biomarker potential.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Primary cilium disassembly - from mechanisms to roles in physiology and disease.Journal of cell science · 2026Review
- TTBK2-Driven Ciliogenesis Is Required for Intrinsic Neuronal Regeneration After Spinal Cord Injury.CNS neuroscience & therapeutics · 2026Article
- Phosphorylation at the Helm: Kinase-Mediated Regulation of Primary Cilia Assembly and Disassembly.Cytoskeleton (Hoboken, N.J.) · 2025Review
- Coordinated roles of the CEP164 homodimer and TTBK2 are required for recruitment of the IFT machinery to the mother centriole for ciliogenesis.Molecular biology of the cell · 2025Article
- Cilia at the crossroad: convergence of regulatory mechanisms to govern cilia dynamics during cell signaling and the cell cycle.Cell & bioscience · 2025Review
- Tubulin detyrosination shapesProceedings of the National Academy of Sciences of the United States of America · 2025Article
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Authors and funding
9 authors.
Funding
Abstract
backgroundPrimary cilia facilitate cellular signalling and play critical roles in development, homeostasis, and disease. Their assembly is under the control of Tau-Tubulin Kinase 2 (TTBK2), a key enzyme mutated in patients with spinocerebellar ataxia. Recent work has implicated TTBK2 in the regulation of cilia maintenance and function, but the underlying molecular mechanisms are not understood.
methodsTo dissect the role of TTBK2 during cilia growth and maintenance in human cells, we examined disease-related TTBK2 truncations. We used biochemical approaches, proteomics, genetic engineering, and advanced microscopy techniques to unveil molecular events triggered by TTBK2.
resultsWe demonstrate that truncated TTBK2 protein moieties, unable to localize to the mother centriole, create unique semi-permissive conditions for cilia assembly, under which cilia begin to form but fail to elongate. Subsequently, we link the defects in cilia growth to aberrant turnover of a microtubule-depolymerizing kinesin KIF2A, which we find restrained by TTBK2 phosphorylation.
conclusionsTogether, our data imply that the regulation of KIF2A by TTBK2 represents an important mechanism governing cilia elongation and maintenance. Further, the requirement for concentrating TTBK2 activity to the mother centriole to initiate ciliogenesis can be under specific conditions bypassed, revealing TTBK2 recruitment-independent functions of its key partner, CEP164.
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