The junctional and centrosome defects in obe mutants are rescued by inhibiting microtubule polymerization. (A–D) Wild-type (WT) embryos (A and B) and obe1/obe2 mutants (C and D) at stage 7, either mock treated (A and C) or incubated for 7 min in 56-nM nocodazole immediately before fixation (B and D). Centrosomes (Cnn) moved to a lateral position basal to the Par-3 plane, and Par-3 was distributed along horizontal cell interfaces in mock-treated and nocodazole-treated wild-type embryos (n = 7–10 embryos per condition). In untreated obe mutants, centrosomes remained in the same plane as Par-3 aggregates. Centrosome positioning and Par-3 localization were restored to wild type in nocodazole-treated obe mutants (n = 13–15 embryos per condition). (E) Percentage of embryos with wild-type Par-3 localization (no aggregates) and centrosomes that were correctly positioned laterally. In mock-treated embryos, 87% of obe mutants had Par-3 aggregates compared with 11% of wild-type controls (***, P = 0.0008 by unpaired t test). In nocodazole-treated embryos, 13% of obe mutants had Par-3 aggregates compared with 16% of wild-type controls (n.s., P = 0.72). Means ± SEM between experiments are shown. The obe1/obe2 mutant embryos were the progeny of obe1/obe2 females crossed to obe2/+ males. Anterior left, dorsal up. Bar, 10 µm. See also Fig. S2.
