ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
A Cdk5-dependent switch regulates Lis1/Ndel1/dynein-driven organelle transport in adult axons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.
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Who cites it
83 citing papers in PubMed, 115 citations in OpenAlex.
- HDAC6 inhibition alleviates mitochondrial trafficking in models of Charcot-Marie-Tooth disease type 2A.JCI insight · 2026Article
- PACS1 syndrome mutation disrupts dynein-mediated cargo transport via HDAC6 and BICD2.Communications biology · 2026Article
- 14-3-3θ phosphorylation at S232 reduces its interactome and regulates axonal trafficking.Disease models & mechanisms · 2025Article
- A novel 14-3-3θ phosphomimetic mouse model demonstrates social dominance defects.Biology open · 2025Article
- Systems mapping of bidirectional endosomal transport through the crowded cell.Current biology : CB · 2024Article
- The Role of Nde1 phosphorylation in interkinetic nuclear migration and neural migration during cortical development.Molecular biology of the cell · 2024Article
- Molecular mechanism of dynein-dynactin complex assembly by LIS1.Science (New York, N.Y.) · 2024Article
- Mitigating aberrant Cdk5 activation alleviates mitochondrial defects and motor neuron disease symptoms in spinal muscular atrophy.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Nde1 promotes Lis1-mediated activation of dynein.Nature communications · 2023Article
- Nde1 Promotes Lis1-Mediated Activation of Dynein.bioRxiv : the preprint server for biology · 2023Article
- LIS1 RNA-binding orchestrates the mechanosensitive properties of embryonic stem cells in AGO2-dependent and independent ways.Nature communications · 2023Article
- Ndel1 disfavors dynein-dynactin-adaptor complex formation in two distinct ways.The Journal of biological chemistry · 2023Article
- The meiotic LINC complex component KASH5 is an activating adaptor for cytoplasmic dynein.The Journal of cell biology · 2023Article
- Ndel1 modulates dynein activation in two distinct ways.bioRxiv : the preprint server for biology · 2023Article
- RAGE activation in macrophages and development of experimental diabetic polyneuropathy.JCI insight · 2022Article
- LRRK1-mediated NDEL1 phosphorylation promotes cilia disassembly via dynein-2-driven retrograde intraflagellar transport.Journal of cell science · 2022Article
- Nde1 and Ndel1: Outstanding Mysteries in Dynein-Mediated Transport.Frontiers in cell and developmental biology · 2022Review
- LIS1 and NDEL1 Regulate Axonal Trafficking of Mitochondria in Mature Neurons.Frontiers in molecular neuroscience · 2022Article
- Long-distance regressive signaling in neural development and disease.Wiley interdisciplinary reviews. Developmental biology · 2021Review
- Article
23 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Lissencephaly is a human developmental brain abnormality caused by LIS1 haploinsufficiency. This disorder is in large part attributed to altered mitosis and migration in the developing brain. LIS1 and an interacting protein, NDEL1, bind to cytoplasmic dynein, a microtubule motor protein. While the tripartite complex is clearly important for developmental events, we are intrigued by the fact that Lis1 and Ndel1 expression remain high in the adult mouse nervous system. Dynein plays a crucial role in retrograde axonal transport, a process that is used by mature neurons. Here, we monitored acidic organelles moving in axons of adult rat sensory neurons to determine whether Lis1 and Ndel1 contribute to axonal transport. Lis1 RNAi significantly reduced axon transport of these organelles. Ndel1 RNAi had little impact, but combined Lis1 and Ndel1 RNAi caused a more severe phenotype than Lis1 RNAi alone, essentially shutting down transport. Lis1 overexpression stimulated retrograde transport, while a Lis1 dynein-binding mutant severely disrupted transport. Overexpression of Ndel1 or a Lis1 Ndel1-binding mutant only mildly perturbed transport. However, expressing a mutant Ndel1 lacking key phosphorylation sites shut down transport completely, as did a dominant-negative Cdk5 construct. We propose that, in axons, unphosphorylated Ndel1 inhibits the capacity of dynein to transport acidic organelles. Phosphorylation of Ndel1 by Cdk5 not only reduces this inhibition but also allows Lis1 to further stimulate the cargo transport capacity of dynein. Our data raise the possibility that defects in a Lis1/Ndel1 regulatory switch could contribute to neurodegenerative diseases linked to axonal pathology in adults.
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