ArticleThe Journal of cell biology2007
Control of nuclear centration in the C. elegans zygote by receptor-independent Galpha signaling and myosin II.
Article in The Journal of cell biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed.
- Active fluctuations of cytoplasmic actomyosin networks facilitate dynein-driven transport.iScience · 2025Article
- Dynein localization and pronuclear movement in the C. elegans zygote.Cytoskeleton (Hoboken, N.J.) · 2022Article
- The coordination of spindle-positioning forces during the asymmetric division of the Caenorhabditis elegans zygote.EMBO reports · 2021Article
- The Generation of Dynein Networks by Multi-Layered Regulation and Their Implication in Cell Division.Frontiers in cell and developmental biology · 2020Review
- Eph signaling controls mitotic spindle orientation and cell proliferation in neuroepithelial cells.The Journal of cell biology · 2019Article
- Cytoplasmic flows as signatures for the mechanics of mitotic positioning.Molecular biology of the cell · 2017Article
- Loss of Gα12/13 exacerbates apical area dependence of actomyosin contractility.Molecular biology of the cell · 2016Article
- Mitotic Spindle Positioning in the EMS Cell of Caenorhabditis elegans Requires LET-99 and LIN-5/NuMA.Genetics · 2016Article
- Moving and positioning the nucleus in skeletal muscle - one step at a time.Nucleus (Austin, Tex.) · 2015Review
- Evolutionary comparisons reveal a positional switch for spindle pole oscillations in Caenorhabditis embryos.The Journal of cell biology · 2013Article
- The branched actin nucleator Arp2/3 promotes nuclear migrations and cell polarity in the C. elegans zygote.Developmental biology · 2011Article
- aPKC phosphorylates NuMA-related LIN-5 to position the mitotic spindle during asymmetric division.Nature cell biology · 2011Article
- Intracellular organelles mediate cytoplasmic pulling force for centrosome centration in the Caenorhabditis elegans early embryo.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- CAMDI, a novel disrupted in schizophrenia 1 (DISC1)-binding protein, is required for radial migration.The Journal of biological chemistry · 2010Article
- Ablation of nonmuscle myosin II-B and II-C reveals a role for nonmuscle myosin II in cardiac myocyte karyokinesis.Molecular biology of the cell · 2010Article
- Membrane invaginations reveal cortical sites that pull on mitotic spindles in one-cell C. elegans embryos.PloS one · 2010Article
- Linear arrays of nuclear envelope proteins harness retrograde actin flow for nuclear movement.Science (New York, N.Y.) · 2010Article
- LET-99 inhibits lateral posterior pulling forces during asymmetric spindle elongation in C. elegans embryos.The Journal of cell biology · 2010Article
- Regulation of cortical contractility and spindle positioning by the protein phosphatase 6 PPH-6 in one-cell stage C. elegans embryos.Development (Cambridge, England) · 2010Article
- Spindle orientation during asymmetric cell division.Nature cell biology · 2009Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Mitotic spindle positioning in the Caenorhabditis elegans zygote involves microtubule-dependent pulling forces applied to centrosomes. In this study, we investigate the role of actomyosin in centration, the movement of the nucleus-centrosome complex (NCC) to the cell center. We find that the rate of wild-type centration depends equally on the nonmuscle myosin II NMY-2 and the Galpha proteins GOA-1/GPA-16. In centration- defective let-99(-) mutant zygotes, GOA-1/GPA-16 and NMY-2 act abnormally to oppose centration. This suggests that LET-99 determines the direction of a force on the NCC that is promoted by Galpha signaling and actomyosin. During wild-type centration, NMY-2-GFP aggregates anterior to the NCC tend to move further anterior, suggesting that actomyosin contraction could pull the NCC. In GOA-1/GPA-16-depleted zygotes, NMY-2 aggregate displacement is reduced and largely randomized, whereas in a let-99(-) mutant, NMY-2 aggregates tend to make large posterior displacements. These results suggest that Galpha signaling and LET-99 control centration by regulating polarized actomyosin contraction.
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