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Figure 9 | BMC Evolutionary Biology

Figure 9

From: The tiny Hairless protein from Apis mellifera: a potent antagonist of Notch signaling in Drosophila melanogaster

Figure 9

A.m.H antagonizes many different Notch-dependent processes during appendage 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) Notch signaling is required for proximo-distal patterning of the leg, notably the formation of segmental joints. Ptc-Gal4 drives H expression in all larval discs along the antero-posterior border. One consequence is the repression of Notch signaling during leg development, causing fusion of the otherwise separated tarsomeres (t1–t5, arrow in B and C) of the tarsus. Moreover, femur (fem) and tibia (tib) are not well separated. D-F) Overexpression of D.m.H and A.m.H in the ptc pattern leads to split halteres (arrow in E and F). G-K) During wing development, Notch is required for outgrowth of the wing blade, margin formation and establishment and refinement of the veins. G) Control wing. H, I) The distance between the third and fourth longitudinal wing veins is conspicuously reduced upon overexpression of D.m.H along the antero-posterior border (ptc-Gal4). In addition, a gap is seen in the distal wing margin (arrow). I) The former phenotype is less pronounced using A.m.H (double arrow; compare with H). Hence, the wing incision appears larger (arrow). J, K) Ap-Gal4 drives H expression in the dorsal compartment, resulting in broadened veins (arrows) and smaller dorsal surface causing blisters (open arrows).

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