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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.
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