ArticleProceedings of the National Academy of Sciences of the United States of America2009
Neurodegeneration mutations in dynactin impair dynein-dependent nuclear migration.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 79 citations in OpenAlex.
- Article
- Control of motor landing and processivity by the CAP-Gly domain in the KIF13B tail.Nature communications · 2023Article
- Multiple roles for the cytoskeleton in ALS.Experimental neurology · 2022Review
- A novel variant inCold Spring Harbor molecular case studies · 2022Review
- Hierarchical integration of mitochondrial and nuclear positioning pathways by the Num1 EF hand.Molecular biology of the cell · 2022Article
- The microtubule-associated protein She1 coordinates directional spindle positioning by spatially restricting dynein activity.Journal of cell science · 2021Article
- On and off controls within dynein-dynactin on native cargoes.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Interplay of Disorder and Sequence Specificity in the Formation of Stable Dynein-Dynactin Complexes.Biophysical journal · 2020Article
- DYNLRB1 is essential for dynein mediated transport and neuronal survival.Neurobiology of disease · 2020Article
- Help or hindrance: how do microtubule-based forces contribute to genome damage and repair?Current genetics · 2020Review
- Setting the dynein motor in motion: New insights from electron tomography.The Journal of biological chemistry · 2019Review
- Molecular basis for dyneinopathies reveals insight into dynein regulation and dysfunction.eLife · 2019Article
- Astral microtubule forces alter nuclear organization and inhibit DNA repair in budding yeast.Molecular biology of the cell · 2019Article
- Nuclear movement in fungi.Seminars in cell & developmental biology · 2018Review
- Cortical dynein pulling mechanism is regulated by differentially targeted attachment molecule Num1.eLife · 2018Article
- She1 affects dynein through direct interactions with the microtubule and the dynein microtubule-binding domain.Nature communications · 2017Article
- Mitochondria-driven assembly of a cortical anchor for mitochondria and dynein.The Journal of cell biology · 2017Article
- Microtubule cross-linking activity of She1 ensures spindle stability for spindle positioning.The Journal of cell biology · 2017Article
- Dynein is regulated by the stability of its microtubule track.The Journal of cell biology · 2017Article
- Dynactin binding to tyrosinated microtubules promotes centrosome centration in C. elegans by enhancing dynein-mediated organelle transport.PLoS genetics · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Neurodegenerative disease in humans and mice can be caused by mutations affecting the microtubule motor dynein or its biochemical regulator, dynactin, a multiprotein complex required for dynein function (1-4). A single amino acid change, G59S, in the conserved cytoskeletal-associated protein glycine-rich (CAP-Gly) domain of the p150(glued) subunit of dynactin can cause motor neuron degeneration in humans and mice, which resembles ALS (2, 5-8). The molecular mechanism by which G59S impairs the function of dynein is not understood. Also, the relevance of the CAP-Gly domain for dynein motility has not been demonstrated in vivo. Here, we generate a mutant that is analogous to G59S in budding yeast, and show that this mutation produces a highly specific phenotype related to dynein function. The effect of the point mutation is identical to that of complete loss of the CAP-Gly domain. Our results demonstrate that the CAP-Gly domain has a critical role in the initiation and persistence of dynein-dependent movement of the mitotic spindle and nucleus, but it is otherwise dispensable for dynein-based movement. The need for this function appears to be context-dependent, and we speculate that CAP-Gly activity may only be necessary when dynein needs to overcome high force thresholds to produce movement.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.