Promotion of the aster-cortex interaction facilitates the formation of the bidirectional cortical flow. Further evidence of the acceleration of the formation of the bidirectional cortical flow and the initial furrowing. (A) Stills from a video sequence of an embryo expressing myosin II-GFP depleted of CYK-4, the GAP subunit of centralspindlin, in which the central spindle was ruptured (yellow arrowheads) due to defective microtubule bundling, allowing earlier approach of the spindle poles to the polar cortexes. The initial sign of furrowing (green arrows) was detected earlier than in the control embryos (see Fig. 2 C for statistics), but the furrow failed to deepen. (B and C) Density (top) and flow (bottom) of the cortical myosin II. (B) In addition to the microtubule-bundling activity, centralspindlin has been shown to interact with a RhoGEF, ECT2, and to promote the activity of the actomyosin network. This activity is partially redundant with another upstream activator of ECT2, NOP-1. Consistent with the earlier formation of the furrow (A; Fig. 2 C), depletion of CYK-4 accelerated the timing of the formation of the bidirectional cortical flow (white dashed line). In contrast, in the embryos depleted of NOP-1, the timing of the formation of the bidirectional flow was not affected, although the flow from the posterior to anterior was weaker and the timing of initial furrowing was delayed (Fig. 2 C). (C) The aster-cortex interaction is known to be regulated by a microtubule depolymerizer, KLP-7/MCAK, and by a negative regulator of the cortical dynein, EFA-6. In the embryos depleted of either of them, the bidirectional flow formed earlier than in the control embryos, consistent with the earlier initial sign of the furrow formation (Fig. 2 C).