Fig. 7. Functional dissection of the Slp binding sites in the bap enhancer. (A) Wild-type and mutated sequences within the region protected by Slp. The inverted repeat of canonical forkhead domain-binding motifs is in black boxes and the CAAA type of Slp-binding motifs are underlined in red. Unaltered sequences are represented by dashes below, and deleted sequences are indicated as a bracketed unbroken line. (B) Activity of the parental bap3.2.1-lacZ construct used as a control. (C) bap3.2.1-slp-m1-lacZ is not active in the mesoderm, while in the dorsal ectoderm it is active in metameric domains and there is weak ectopic activity between these domains. (D) bap3.2.1-slp-m2-lacZ shows very weak activity in the mesoderm and similar ectodermal activity as with bap3.2.1-slp-m1-lacZ. (E) bap3.2.1-slp-m3-lacZ shows weakened activity in the mesoderm and similar ectodermal activity as with bap3.2.1-lacZ. (F) bap3.2.1-slp-m4-lacZ activity is similar to that of the parental bap.3.2.1-lacZ (mesodermal clusters have physically merged at this slightly later stage). (G) bap3.2.1-slp-m5-lacZ shows lack of mesodermal activity and largely uniform dorsal ectodermal activity along the anteroposterior axis. (H,I) Fluorescent double staining for Slp (red) and ßGal (green) in stage 10 embryos. bap3.2.1-lacZ expression (H) is complementary to that of Slp, whereas bap3.2.1-slp-d1-lacZ expression (I) overlaps with Slp.