Activities of Gal4-Giant fusion genes. Transgenic
embryos contain either the NEE.UAS-2xPE-lacZ or
NEE.UAS-lacZ reporter gene and different
Krüppel-Gal4-Giant expression vectors. Embryos
were hybridized with either a giant antisense RNA probe
(A) or a lacZ probe
(B–H). (A)
giant staining pattern in a transgenic embryo that
contains the Krüppel-Gal4-Giant (1) fusion
gene. Staining is detected in anterior and posterior regions
(Upper, brackets), which correspond to the
endogenous pattern. The Krüppel
transgene directs strong expression in central regions
(Lower, bracket). (B) The
NEE.UAS-2xPE-lacZ reporter gene in a wild-type embryo
lacking any of the Krüppel-Gal4-Giant expression
vectors. Staining is detected in the ventral mesoderm (white arrowhead)
and in lateral lines in the neurogenic ectoderm (red arrowheads).
(C) Same as B, except that the embryo
also expresses the Gal4-Giant (1) fusion protein. The lateral
staining pattern directed by the modified NEE is repressed in central
regions (arrowheads). In contrast, staining directed by the
twist enhancer (2xPE) is unaffected. (D)
The NEE.UAS-lacZ reporter gene in a wild-type embryo
lacking Krüppel-Gal4-Giant expression vectors. The
lacZ reporter gene exhibits uniform expression in
ventral regions. There is no gap in the center (arrowhead).
(E) Same as D, except that the embryo
also expresses the Gal4-Giant (1) fusion protein. There is a gap
in central regions (arrowhead). (F) Same as
E, except that the embryo expresses a Gal4-Giant fusion
protein containing the minimal Giant repression domain (amino acid
residues 60–133). There is a gap in the staining pattern in central
regions (arrowhead). (G) Same as D,
except that the embryo also expresses a mutant version of the
full-length Gal4-Giant fusion protein with an internal deletion in the
minimal repression domain (Δ60–133). There is no significant
repression of lacZ staining in central regions
(arrowhead). (H) Same as D, except that
the embryo also expresses a mutant form of the Gal4-Giant fusion
protein containing alanine substitutions in the VLDLS motif (see Fig.
3).