Figure 2.
Cytoplasmic transport of myosin II particles and timely furrow formation depend on the astral microtubules and dynein.(A) Embryos expressing NMY-2::GFP were treated with 15 µM nocodazole, a microtubule poison, or the drug vehicle (control) during anaphase (at 0 s). Nocodazole strongly suppressed the cytoplasmic motility of myosin II. (B) Depletion of the cytoplasmic dynein heavy chain (dhc-1(RNAi)) or the dynein regulator LIN-5/NuMA (lin-5(RNAi)) eliminated the cytoplasmic unidirectional movement of myosin II. * indicates the polar body. (C) Timing of the initial sign of furrow formation determined by visual inspection of anonymized videos (mean ± SEM). Statistical significance was tested against the control by linear modeling with correction for multiple comparisons by Dunnett’s method. *, **, and *** indicate P < 0.02, 0.01, and 0.001, respectively.

Cytoplasmic transport of myosin II particles and timely furrow formation depend on the astral microtubules and dynein. (A) Embryos expressing NMY-2::GFP were treated with 15 µM nocodazole, a microtubule poison, or the drug vehicle (control) during anaphase (at 0 s). Nocodazole strongly suppressed the cytoplasmic motility of myosin II. (B) Depletion of the cytoplasmic dynein heavy chain (dhc-1(RNAi)) or the dynein regulator LIN-5/NuMA (lin-5(RNAi)) eliminated the cytoplasmic unidirectional movement of myosin II. * indicates the polar body. (C) Timing of the initial sign of furrow formation determined by visual inspection of anonymized videos (mean ± SEM). Statistical significance was tested against the control by linear modeling with correction for multiple comparisons by Dunnett’s method. *, **, and *** indicate P < 0.02, 0.01, and 0.001, respectively.

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