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Fig. 6. In vivo requirements for binding sites of Smad, Tin and Bap proteins, and
for other conserved sequences. (A) Schematic representations of
bap3.2.1 and its mutated derivatives with a summary of their in vivo
activities (ms, dorsal mesoderm; ec, dorsal ectoderm). (B-I) Dorsal views of
stage 11 embryos. Arrow indicates mesodermal layer and arrowhead indicates
ectodermal layer. (B) Activity of the parental bap3.2.1-lacZ
construct. (C) Mutations in the Bap-binding site cause a slight and transient
reduction of mesodermal enhancer activity. (D) Mutations in the Tin-binding
site cause a loss of enhancer activity in the mesoderm. (E) Mutations in the
Mad/Medea-binding site 1 cause a loss of enhancer activity in both ectoderm
and mesoderm. (F) Mutations in the Mad/Medea-binding site 2 nearly abolish
enhancer activity in both ectoderm and mesoderm. (G) Deletion of DNA sequences
containing the Mad/Medea-binding sites 3 and 4 causes a strong reduction of
ectodermal and mesodermal enhancer activity. (H,I) Mutations within the
conserved sequence C1 of the enhancer from D. melanogaster (H) and
D. virilis (I) cause a loss of enhancer activity in both ectoderm and
mesoderm. (The observed expression within single ectodermally derived cells in
each hemisegment is an artificial effect from the transformation vector.)
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