Fig. 6. Forced expression of UAS sens in Su(H)⁴⁷ mutant wing imaginal discs re-establishes the expression of the SOP-E, hnt, 22C10 and elav in cells of the proneural cluster. Anterior is towards the left, ventral is towards the bottom. (A-G) Expression of UAS sens with dppGal4 in Su(H) mutant wing imaginal discs. (A) Expression of the SOP-E is activated in a stripe of cells (arrow) in the notum that corresponds to the dppGal4 expression domain. (B) Expression of 22C10 (arrow). (C) The same disc as in B showing expression of UASGFP in green and 22C10 in red. The double staining reveals that most of the cells in the notum that express Sens initiate expression of the neurone-specific marker 22C10 (arrow). The arrowhead in A-C indicates the boundary between the notum and the wing and highlights the fact that the ability of Sens to activate the SOP-E and 22C10 is restricted to cells of the notum. (D) Expression of elav revealed by anti Elav staining. (E) The same disc as in D showing the expression of UAS GFP in green and that of Elav in red. The double staining reveals that although Sens is expressed in a broad stripe in the notum, elav expression is activated only in clusters of cells that are located at positions of the proneural clusters (arrows). This observation suggests that other, locally restricted factors are in addition required to initiate the expression of elav. As in the case of 22C10, Sens can activate expression of Hnt in all cells of the notum where it is expressed (see F,G). (F) Expression of Hnt. (G) Expression of UAS GFP (green) and Hnt (red) in the same disc as shown in F. Arrowheads in F and G indicate the wing/notum boundary and that the ability of Sens to activate hnt is again restricted to cells of the notum. (H) Results summary. Sens seems to be required to activate the expression of hnt, and the neurone-specific genes 22C10 and elav in the developing SOP. This suggests that Sens coordinates the development and differentiation of the SOP. Furthermore, Sens seems to be required for the maintenance of the expression of the SOP-E and thus, the maintenance of high proneural gene activity in the SOP. Hence, the results suggest that loss of Sens activity is the cause for the observed arrest in development in Su(H) mutants.