A.m.H antagonizes different Notch-dependent processes during eye and thorax development. D.m.H (central panel, UAS-DmH) and A.m.H (right panel; UAS-AmH) full length constructs were overexpressed in a spatially and temporally controlled manner using the Gal4-UAS system. Controls (left panel) are derived from crosses of the same Gal4-line with UAS-lacZ. A-C) Ey-Gal4 drives expression of H in the developing eye disc. As a consequence of impeded cell proliferation and increased cell death, adult eyes are small or completely absent (arrows). D-F) Gmr-Gal4 drives expression of H behind the morphogenetic furrow, which interferes with the process of photoreceptor and cone cell fate determination, respectively. As a consequence of misspecification of cells and cell death, adult eyes are smaller and have a rough appearance. D'-F') Enlargements show that the regular architecture of ommatidia (see D') is disturbed due to fusions and disarrangement (arrows in E' and F'). Interommatidial bristles (arrowheads in E' and F') are duplicated or lacking. Some ommatidia show signs of cell death (open arrows in E' and F'). G-I) Pnr-Gal4 drives H expression in the central region of the thorax anlagen, which interferes with Notch-mediated dorsal closure. In addition to a smaller size due to impeded cell proliferation and increased cell death, the thorax has a marked cleft (arrow). Note also bristle loss and duplications (open arrow). J, K) Sca-Gal4 drives H expression in proneural clusters, resulting in bristle loss (open arrow), additional and split bristles (arrow), as outlined in Fig. 5.