Supplementary Material
DEV02796 Supplementary Material
Files in this Data Supplement:
- Supplemental Figure 1
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Fig. S1. SoxN loss-of-function cuticle patterns. (A) The SoxNNC14-mutant allele in trans with Df(2L)Exel7040 shows a slight excess of naked cuticle, indistinguishable from that of the homozygous SoxNNC14 mutant. (B) Heterozygosity for Dichaete (D) does not increase the extent of naked cuticle observed in mutant SoxNNC14 embryos, but it does alter the morphology of the denticles (inset). (C) The SoxNGA1192 protein-null allele in trans with Df(2L)Exel7040 shows a cuticle pattern indistinguishable from that of SoxNNC14 over the deficiency (A). However, homozygotes for the SoxNGA1192 chromosome (D) show a substantially more severe loss of denticles, suggesting that the chromosome bears additional mutations that disrupt cuticle deposition. It is formally possible that this allele behaves in an antimorphic (Muller, 1932) fashion, but because no protein product is detected (Buescher et al., 2002) and the mutation does not show any dominance, the increased severity in the homozygous state is more likely to be due to extraneous mutations that are homozygosed along with the SoxN lesion.
- Supplemental Figure 2
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Fig. S2. Overexpression of SoxN does not alter Wg- or Arm-antibody staining. Wg-antibody staining in wild-type w1118 embryos (A) and in embryos derived from crossing the E22C-Gal4 driver with UAS-SoxN (B), show similar levels and patterns of wg gene product. These transgenic lines, in the w1118-mutant background, are homozygous. Therefore, all of the progeny overexpress SoxN at high levels. Arm-antibody staining in wild-type w1118 embryos (C) and in embryos derived from crossing the E22C-Gal4 driver with UAS-SoxN (D), show similar levels and patterns of Arm protein at stage 9. The Arm striping becomes less distinctive at later stages, but no differences in Arm levels are observed in wild-type w1118 embryos (E) and embryos derived from crossing the E22C-Gal4 driver with UAS-SoxN (F), at stage 11.
