Figure 6. PCM becomes fracture resistant... | Rockefeller University Press

Figure 6.

$PCM becomes fracture resistant and ductile in anaphase after inhibition of PP2A phosphatase. (A) PCM was subjected to high-flow FLUCS during anaphase in wild-type embryos or permeabilized embryos treated with 10 µM LB-100 (inhibitor of PP2A phosphatase). (B) PCM deformation rates in anaphase using high flow in wild-type and LB-100–treated embryos. Wild-type data are from experiments in Fig. 1. Individual data points are plotted with bars representing mean ± 95% CI; n = 7 (wild-type) and 10 (LB-100-treated) centrosomes. P values were calculated using a Mann–Whitney U test. (C) Ratio of final PCM length to original length in experiments from B. Original PCM length was measured before flow began, and final PCM length was measured once flow was turned off. P values were calculated using a Mann–Whitney U test. (D) PCM fracture probabilities for high-flow FLUCS in metaphase (M), anaphase (A), and telophase (T). Wild-type data are from experiments in Fig. 1; n = 8, 11, and 11 (wild-type) and 7, 9, and 6 (LB-100-treated) centrosomes. (E) Permeabilized embryos were treated with no drug or 10 µM LB-100 in metaphase and imaged until 300 s after anaphase onset. Data are plotted as normalized lines representing mean ± 95% CI; n = 24 (no drug) and n = 21 (LB-100-treated) centrosomes. (F) Dual-color imaging of embryos expressing GFP-tagged LET-92, the PP2A catalytic subunit in C. elegans (GFP::PP2Ac), and SPD-5::mCherry. Data are plotted as normalized lines representing mean ± 95% CI; n = 10 centrosomes.$

PCM becomes fracture resistant and ductile in anaphase after inhibition of PP2A phosphatase. (A) PCM was subjected to high-flow FLUCS during anaphase in wild-type embryos or permeabilized embryos treated with 10 µM LB-100 (inhibitor of PP2A phosphatase). (B) PCM deformation rates in anaphase using high flow in wild-type and LB-100–treated embryos. Wild-type data are from experiments in Fig. 1. Individual data points are plotted with bars representing mean ± 95% CI; n = 7 (wild-type) and 10 (LB-100-treated) centrosomes. P values were calculated using a Mann–Whitney U test. (C) Ratio of final PCM length to original length in experiments from B. Original PCM length was measured before flow began, and final PCM length was measured once flow was turned off. P values were calculated using a Mann–Whitney U test. (D) PCM fracture probabilities for high-flow FLUCS in metaphase (M), anaphase (A), and telophase (T). Wild-type data are from experiments in Fig. 1; n = 8, 11, and 11 (wild-type) and 7, 9, and 6 (LB-100-treated) centrosomes. (E) Permeabilized embryos were treated with no drug or 10 µM LB-100 in metaphase and imaged until 300 s after anaphase onset. Data are plotted as normalized lines representing mean ± 95% CI; n = 24 (no drug) and n = 21 (LB-100-treated) centrosomes. (F) Dual-color imaging of embryos expressing GFP-tagged LET-92, the PP2A catalytic subunit in C. elegans (GFP::PP2Ac), and SPD-5::mCherry. Data are plotted as normalized lines representing mean ± 95% CI; n = 10 centrosomes.

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