Fig. 2

Cortical movement of Bcd and how drugs affect movement and stability of the Bcd protein. Pictures represent midsagittal confocal planes of bcd^{+ 5 + 8} embryos [20] that produce 3 times more Bcd protein than in wild-type, oriented with their dorsal side up and anterior to the left. Relative intensities of the crude confocal pictures were converted to a color scale with values of 0–255 (8-bit), shown in insert of (f). Nomenclature of nuclear cycles (in green) follows that of [28]. Red areas in (a-d, f) represents the yolk. a untreated nuclear cycle (nc) 4 embryo showing the majority of the Bcd protein at the tip and a small gradient is observed. The yolk part (red) serves as a non-permissive territory for Bcd which refutes the SDD model (Fig. 1e). b untreated nc 8 embryo showing the Bcd protein moving along the cortex to the posterior. The yolk part (red) serves as a non-permissive territory. (c, d) nc 6 embryos exposed to hypoxia and “sleeping” [20] for 3 h (c) or 7 h (d), Bcd still moves along the cortex. Under hypoxic conditions, the yolk (red) still serves as non-permissive territory of Bcd movement. e nc 6 embryo exposed to vinblastine affecting microtubular (MT) stability, the yolk becomes permissive and Bcd moves to the posterior in a broad front (blue arrows), as the SDD model would have predicted (Fig. 1e). (f) nc 6 embryo exposed to latrunculin B affecting actin structures, the stability of Bcd is strongly affected, as well as posterior movement is slowed down. The yolk (red) still retains its non-permissiveness