The DOI matches its Crossref record; 28 of the 28 references it cites were found in a registry or an index.
The Drosophila ncd microtubule motor protein is spindle-associated in meiotic and mitotic cells
Abstract
The nonclaret disjunctional (ncd) protein is required for normal chromosome distribution in oocytes and early embryos. Mutants of ncd cause frequent nondisjunction and loss of chromosomes, suggesting a role for the protein in spindle function or chromosome movement in meiosis and early mitosis. The ncd protein contains a region of predicted sequence similarity to the microtubule motor protein, kinesin. In vitro motility assays have demonstrated that ncd is a motor that unexpectedly moves toward the minus ends of microtubules, opposite to the direction of kinesin movement. Using antibodies directed against nonconserved regions of the protein, we have localized the ncd motor protein to the meiotic and early mitotic spindle, and to spindles in a mitotically dividing cultured cell line. Its presence in the spindle of meiotic and mitotic cells implies a role for the protein as a spindle motor. The motor may play an essential role in establishing spindle bipolarity in meiosis.
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“The second role is to organize spindle MTs at MT minus ends and focus them into spindle poles (5)(6)(7).”
From Diffusion and Directed Movement (2008) · cites this paper as [5]
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Research works printed but not linked: 1
- O’Tousa, 1980, The initial characterization of non-claret disjunctional (ncd): evidence that cand is the double mutant, ca ncd, Dros. Inf. Serv, 55, 119
Cited by
Wordeman, L., & Mitchison, T. J. (1995) · The Journal of cell biology · doi:10.1083/jcb.128.1.95 · Cited by 382
Centrosome Reduction During Gametogenesis and Its Significance1
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The Road Less Traveled: Emerging Principles of Kinesin Motor Utilization
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Metadata
- Authors
- Hatsumi, M., & Endow, S. A.
- Affiliations
- Duke Medical Center (US)
- ORCID
- Endow, Sharyn A.
- Venue
- Journal of Cell Science
- Publisher
- The Company of Biologists
- Published
- 1992-12-01
- Volume
- 103
- Issue
- 4
- Pages
- 1013-1020
- ISSN
- 0021-9533 (ISSN-L)
- 1477-9137
- OpenAlex
- W2106258850
- Cited by
- 92
- References
- 28
- Citations by year
- 2026: 1 · 2024: 1 · 2022: 1 · 2020: 4 · 2019: 1 · 2018: 4 · 2017: 1 · 2016: 1 · 2015: 2 · 2013: 1 · 2012: 1
- FWCI
- 2.05
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Cell Science (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of General Medical Sciences (R01GM046225)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Microtubule and mitosis dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Chromosomal and Genetic Variations
- Keywords
- microtubule motor proteins, kinesin, meiosis, mitosis, nondisjunction, chromosome segregation, spindle bipolarity, oocytes, early embryonic development, minus-end-directed motility
- MeSH terms
- Amino Acid Sequence, Animals, Cells, Cultured, Drosophila melanogaster, Embryo, Nonmammalian, Fluorescent Antibody Technique, Meiosis, Microtubule Proteins, Microtubules, Mitosis, Spindle Apparatus, Molecular Sequence Data, Oocytes, Peptide Fragments, Rabbits, Kinesins, Drosophila Proteins
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- CoChat. (2026). Citation check: The Drosophila ncd microtubule motor protein is spindle-associated in meiotic and mitotic cells. https://app.cochat.ai/papers/10.1242/jcs.103.4.1013
- The paper
- Hatsumi, M., & Endow, S. A. (1992). The Drosophila ncd microtubule motor protein is spindle-associated in meiotic and mitotic cells. Journal of Cell Science. https://doi.org/10.1242/jcs.103.4.1013
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.