Figure 6. Distribution of NMY-2 aggregate displacements along the AP axis. Normalized histograms of AP displacements of NMY-2 aggregates at a time scale of 12 s for each octant of wild-type, zyg-9(or634ts), goa-1(RNAi);gpa-16(RNAi), and let-99(or513ts) zygotes. Tick marks = 1 μm. Displacements of >1 μm are shaded, and the cumulative frequency of >1-μm displacements in each direction is indicated. at http://www.jcb.org/cgi/content/full/jcb.200703159/DC1; and unpublished data). Although the relative density of NMY-2 in the anterior cap was slightly reduced in both mutants, we thought it was unlikely that LET-99 and Ga exert their disparate influ- ences on centration through similar requirements for polarized NMY-2 enrichment. Instead, a slightly flattened profile of NMY-2 intensity could result in each case from an abnormal pattern of NMY-2 aggregate displacements. Therefore, we examined these displacements in goa-1;gpa-16(RNAi) (n = 9) and let-99(or513ts) zygotes (n = 11). In striking contrast to wild type, the AP displacements in cortical regions near and anterior to the NCC in Gα-depleted zygotes were distributed symmetrically at about zero, suggest- ing random movement (Fig. 6). However, in the two posterior octants (d and h), the major peaks were biased toward the pos- terior, indicating that actomyosin movement is not completely randomized by GOA-1/GPA-16 depletion. Also reflecting non- random behavior, large displacements (>1 μm/12 s) were prom- inently biased toward the NCC in regions both to its anterior (b and f) and its posterior (d and h; see Discussion). A different abnormal pattern of biased displacement along the AP axis was detected in let-99(−) zygotes (Fig. 6). In all four central octants (b, c, f, and g), displacements showed a characteristically abnormal profile, with peaks offset further 1184 JCB • VOLUME 178 • NUMBER 7 • 2007