Figure 3.—

alph alleles enhance thorax closure defects generated by Slpr expression. The pannier-Gal4 (pnr-Gal4) driver was used to direct expression of wild-type slpr (pnr>slpr^WT) in dorsal tissues during development. Modulation of thorax defects was evaluated for each heterozygous allele. (A–E) A representative image is shown for each genotype. A wild-type thorax is shown in A. (F) Quantification of thorax closure defects by monitoring the number of scutellar bristles. Wild-type flies have four scutellar bristles while mutants with thorax closure defects generally lose a few or entirely lack these bristles. In an otherwise wild-type (+/+) background, Slpr overexpression generates a thorax closure defect that is accompanied by the loss of one to two bristles with a penetrance of ∼50%. Moreover, this genotype occasionally displays more than four bristles. This was also observed in the hep heterozygous background. The total number of flies scored for each genotype was as follows: pnr>slpr (94); pnr>slpr, hep⁶⁹⁹/+ (41); pnr>slpr, alph^S-331/+ (125); pnr>slpr, alph^XS-88/+ (40); pnr>slpr, puc^E69/+ (6). Owing to a significantly low rate of eclosion, only six adult flies were recovered for the pnr>slpr, puc^E69/+ genotype.