Fig. 10. En requires exd/hth to repress endogenous targets, but only at the anterior of the germ band. Embryos shown at the top (A, B, C) are all deficient for exd (or hth) and, in all panels, En is expressed under the control of paired-Gal4 (e.g. in T2 and A1). (A) In hth^-, expression of ci is repressed by En in A1 but not in T2. In this embryo, all En originates from the transgene since endogenous expression decays in hth mutants. (A') For comparison, the effect of ectopic En on ci expression in hth⁺ is reproduced from Fig. 1B (showing only the left side of the embryo). (B) As with ci, expression of slp is repressed in A1 but not in T2 in exd^- embryos. Here ectopic En is shown in ochre (as detected with an antibody) and slp expression is in blue. Note that in A1, En is present but not slp. (B') Again, for comparison, we show the effect of En expression on slp expression in an otherwise wild type embryo (as in Fig. 5B). (C) In exd mutants, activation of hh expression by En is abolished in both T2 and A1. Here, En protein is shown in ochre and expression of hh is shown in brown. Residual expression (a probable remnant of previous activation by pair-rule gene products) is seen in the normal domain, but not ectopically as happens if exd⁺ is present (shown in C'). (C') Expression of hh is activated in T2 and A1 of otherwise wild type embryos (as shown previously in Fig. 1D).