ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Doublecortin (Dcx) family proteins regulate filamentous actin structure in developing neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
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Who cites it
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.
- Connecting DCX, COMT and FMR1 in social behavior and cognitive impairment.Behavioral and brain functions : BBF · 2022Pooled it
- Cytoskeletal Proteins and Alzheimer's Disease Pathogenesis: Focusing on the Interplay with Tau Pathology.Biomolecules · 2025Review
- Doublecortin restricts neuronal branching by regulating tubulin polyglutamylation.Nature communications · 2025Article
- Emerging roles for E3 ubiquitin ligases in neural development and disease.Frontiers in cell and developmental biology · 2025Review
- Doublecortin-like kinase is required for cnidocyte development in Nematostella vectensis.Neural development · 2024Article
- Cullin-RING E3 ubiquitin ligase 4 regulates neurite morphogenesis during neurodevelopment.iScience · 2024Article
- Netrin-1 stimulated axon growth requires the polyglutamylase TTLL1.Frontiers in neuroscience · 2024Article
- Tunable hydrogel viscoelasticity modulates human neural maturation.Science advances · 2023Article
- Proteomic investigation of neural stem cell to oligodendrocyte precursor cell differentiation reveals phosphorylation-dependent Dclk1 processing.Cellular and molecular life sciences : CMLS · 2023Article
- Zn2+ decoration of microtubules arrests axonal transport and displaces tau, doublecortin, and MAP2C.The Journal of cell biology · 2023Article
- Structure-Guided Prediction of the Functional Impact of DCLK1 Mutations on Tumorigenesis.Biomedicines · 2023Review
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- Visualising the cytoskeletal machinery in neuronal growth cones using cryo-electron tomography.Journal of cell science · 2022Article
- Pleiotropic effects of DCLK1 in cancer and cancer stem cells.Frontiers in molecular biosciences · 2022Review
- Precursor types predict the stability of neuronal branches.Journal of cell science · 2021Article
- Cytoskeleton and Associated Proteins: Pleiotropic JNK Substrates and Regulators.International journal of molecular sciences · 2021Review
- Oleoylethanolamide Delays the Dysfunction and Death of Purkinje Cells and Ameliorates Behavioral Defects in a Mouse Model of Cerebellar Neurodegeneration.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Article
- Role of agmatine in the application of neural progenitor cell in central nervous system diseases: therapeutic potentials and effects.Anatomy & cell biology · 2021Review
- Doublecortin facilitates the elongation of the somatic Golgi apparatus into proximal dendrites.Molecular biology of the cell · 2021Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Doublecortin (Dcx) is the causative gene for X-linked lissencephaly, which encodes a microtubule-binding protein. Axon tracts are abnormal in both affected individuals and in animal models. To determine the reason for the axon tract defect, we performed a semiquantitative proteomic analysis of the corpus callosum in mice mutant for Dcx. In axons from mice mutant for Dcx, widespread differences are found in actin-associated proteins as compared with wild-type axons. Decreases in actin-binding proteins α-actinin-1 and α-actinin-4 and actin-related protein 2/3 complex subunit 3 (Arp3), are correlated with dysregulation in the distribution of filamentous actin (F-actin) in the mutant neurons with increased F-actin around the cell body and decreased F-actin in the neurites and growth cones. The actin distribution defect can be rescued by full-length Dcx and further enhanced by Dcx S297A, the unphosphorylatable mutant, but not with the truncation mutant of Dcx missing the C-terminal S/P-rich domain. Thus, the C-terminal region of Dcx dynamically regulates formation of F-actin features in developing neurons, likely through interaction with spinophilin, but not through α-actinin-4 or Arp3. We show with that the phenotype of Dcx/Doublecortin-like kinase 1 deficiency is consistent with actin defect, as these axons are selectively deficient in axon guidance, but not elongation.
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Registered trials
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