Epistatic relationship between JAK/STAT, Wnt, Hh and Hox inputs over sna-rg regulation.

(A-C) Embryos expressing sna-rg-GFP (green) and vvl1+2-mCherry (red) stained with anti-En (blue). (A) sna-rg and vvl1+2 expression in st11 control embryos. Panels (A’) and (A”) show each channel separately to appreciate the co-expression of both markers in the gland primordia. (B) Df(1)os1A embryos show an almost complete downregulation of sna-rg and vvl1+2 expression from the CA and PG (asterisks). (C) Ectopic Upd expression driven with sal-Gal4 induces ectopic sna-rg and vvl1+2 expression in the gnathal segments, which for sna-rg is more pronounced in the labium than in the maxilla. Note that in the maxillary segment Upd can induce ectopic dorsal vvl1+2 but not sna-rg expression, this is expected as Dfd only induces sna-rg ventrally in the maxilla. (D-E) sna-rg-GFP embryos stained with anti-GFP (green) and anti-Sal (red). In control embryos (D) Sal labels the PG primordium but not the CA. In arm-Gal4 embryos ectopically expressing Upd (E), the PG is more expanded than the CA as shown by the number of cells co-expressing Sal and GFP. (F-G) sna-rg-GFP expression (green) in st13 Dfd Scr mutant embryos (F), or Dfd Scr mutant embryos after ectopic Upd expression driven with the sal-Gal4 line (G) showing that Upd activation is not sufficient to rescue gland formation in Dfd Scr mutants. In Dfd Scr mutant embryos (F), although the gland primordia become apoptotic, residual GFP expression indicates that there must exist Hox independent inputs activating the sna-rg enhancer. Embryos in (F-G) are also stained with anti-Scr to recognise the homozygous mutants. Scale bars 50 μm.