Figure 3
Influence of fusion topologies on abdominalA (AbdA) and extradenticle (Exd) functions in vivo. (a) Cuticle phenotypes of abdA mutants (homozygous for PabdA-Gal4) and rescue activities by AbdA fusion proteins. Mutant larvae are characterized by the loss of denticle rows in A2-A7 segments, presenting a thinner A1-like organization. Enlargements are focused on the A1-A3 segments. Expression of AbdA or VCA in this mutant context restores the A2-like shape of denticle rows. Expression of VNA is less efficient in the rescue, leading to an intermediary A1/A2 organization of denticle belts. Red lines indicate the anterior expression boundary of the abdA-Gal4 driver. (b) Rescue of exd cuticle phenotypes by Exd fusion proteins. In zygotic exdXP11mutant embryos, the T3 segment acquires a mix T1/abdominal identity, while the A1 and A2 segments resemble to more posterior abdominal segments (respectively to A3-like and A4-like segments). The rescue efficiency of Exd fusion proteins was measured in abdominal segments by using the Ultrabithorax(Ubx)-Gal4 driver ([28] and Additional File 1). Abdominal phenotypes were rescued by Exd or VNE and VCE (not shown) fusion proteins. EVC led to an intermediary rescue, with A1 and A2 segments acquiring respectively an A2-like and A3-like morphology. (c) Regulatory effects of AbdA fusion proteins on the Distalless (Dll) enhancer DME [26]. β-Galactosidase (β-Gal) immunostaining (red) reveals the expression of a lacZ reporter gene that is under the control of DME cis-regulatory sequences. Ectopic expression of AbdA (green) in the thoracic T2 segment with the paired (prd)-Gal4 driver led to complete repression of the β-Gal. VCA, and to a lesser extend VNA, are also able to repress DME. Graph on the right shows the statistical quantification of the repression of the β-Gal by AbdA (1), VCA (2) and VNA (3), as deduced from the level of the red fluorescent signal in T2.