期刊
MOLECULAR BIOLOGY OF THE CELL
卷 29, 期 26, 页码 3093-3104出版社
AMER SOC CELL BIOLOGY
DOI: 10.1091/mbc.E17-11-0653
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资金
- NIH Office of Research Infrastructure Programs (University of Minnesota) [P40 OD010440]
- National BioResource Project (Tokyo University, Japan)
- C. elegans Gene Knockout Consortium
- ARC [EML20110602452]
- CNRS
- Rennes Metropole
- Region Bretagne (AniDyn-MT grant)
- CNRS ATIP starting grant
- La Ligue Nationale Contre le Cancer
- COST EU action (GENiE) [BM1408]
- [BIO2013-02]
During asymmetric cell division, the molecular motor dynein generates cortical pulling forces that position the spindle to reflect polarity and adequately distribute cell fate determinants. In Caenorhabditis elegans embryos, despite a measured anteroposterior force imbalance, antibody staining failed to reveal dynein enrichment at the posterior cortex, suggesting a transient localization there. Dynein accumulates at the microtubule plus ends, in an EBP-2EB-dependent manner. This accumulation, although not transporting dynein, contributes modestly to cortical forces. Most dyneins may instead diffuse to the cortex. Tracking of cortical dynein revealed two motions: one directed and the other diffusive-like, corresponding to force-generating events. Surprisingly, while dynein is not polarized at the plus ends or in the cytoplasm, diffusive-like tracks were more frequently found at the embryo posterior tip, where the forces are higher. This asymmetry depends on GPR-1/2LGN and LIN-5NuMA, which are enriched there. In csnk-1(RNAi) embryos, the inverse distribution of these proteins coincides with an increased frequency of diffusive-like tracks anteriorly. Importantly, dynein cortical residence time is always symmetric. We propose that the dynein-binding rate at the posterior cortex is increased, causing the polarity-reflecting force imbalance. This mechanism of control supplements the regulation of mitotic progression through the nonpolarized dynein detachment rate.
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