Fig. 8. Exd and Hth are required for En to activate genes in the abdomen. In all panels, abdominal segments A4 to A8 of es11 embryos are shown. (A) Expression of En protein and hh RNA in an exd deficient embryo. Expression of both En and hh has begun to decay. (B) Transcription of hh in an exd^- embryo expressing exogenous En under the control of the paired-Gal4 driver. No ectopic activation is seen (most ochre cells are not black). There may be slightly increased residual expression of hh (compare black signal in A and B) but this could be in underlying neuroblasts. (C) In the presence of exd⁺, paired-Gal4-driven En activates hh expression through the domain of ectopic expression (see the widening of hh expression in alternate segment as shown for anterior segments in Fig. 1D). (D) Ectopic En does not activate hh expression in a zygotic hth mutant embryo (hth^- paired-Gal4, UAS-en). This shows that a mutation in hth has the same effect as removal of exd (compare with panel B).