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Figure 3


Fig. 3. Epistatic relationships of SoxN with the Wg pathway. (A) The SoxNNC14 mutation placed in trans with a small deficiency for the region, Df(2L)Exel7040, shows no change from the homozygous mutant phenotype (compare with Fig. 2B), indicating that SoxNNC14 behaves as a null allele. (B) Removing maternal SoxN does not increase the severity of the mutant phenotype; therefore, SoxN acts zygotically. (C) Dorsal patterning elements show mild disruptions in some segments of SoxNNC14/Df-mutant embryos (arrow; compare with more anterior segments, which have normal dorsal pattern elements). (D) Overexpressing SoxN in embryos derived from mothers that were heterozygous for groBX22, a deficiency removing the locus, produces milder pattern disruptions both dorsally and ventrally (compare with Fig. 2F). (E,F) Double homozygotes for arm4 and either SoxN allele show the arm `lawn of denticles' phenotype (E), but embryos are smaller and have stronger dorsal pattern disruptions than do arm4 single mutants (F) (data shown in Table 2). (G) Mutants homozygous for SoxN that were derived from groBX22 heterozygous mothers show increased naked cuticle (n=140). (H,I) SoxN; Tcf2 double-mutant embryos also show increased naked cuticle (H). Thus, the SoxN mutant phenotype is epistatic to the Tcf `lawn of denticles' phenotype (I) (data shown in Table 2). (J) E22C-Gal4-driven ubiquitous expression of dominant-negative Tcf produces a `lawn of denticles' phenotype and severely reduces the size of the embryonic cuticle. (K) Segmental patterning and body size of TcfDN-expressing embryos are partially rescued when SoxN dosage is reduced. The SoxNNC14 mutation is linked to the E22C-Gal4 insertion in this experiment, so that all embryos ubiquitously expressing UAS-TcfDN are also heterozygous for SoxN. All show a milder phenotype regardless of whether the SoxN mutation was introduced from the mother or the father (n=205). Embryos are oriented with anterior to the left and dorsal side up.





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