Melissa M. Moline, Herman A. Dierick†, Cozumel Southern, Amy Bejsovec 

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Non-equivalent roles of Drosophila Frizzled and Dfrizzled2 in embryonic Wingless signal transduction  Melissa M. Moline, Herman A. Dierick†, Cozumel Southern, Amy Bejsovec  Current Biology  Volume 10, Issue 18, Pages 1127-1130 (September 2000) DOI: 10.1016/S0960-9822(00)00697-7

Fig. 1 Overexpression of Dfz2, but not fz, restores naked-cuticle specification in wgPE2 mutant embryos. (a) The wg null mutant (wgCX4) phenotype was not altered by overexpressing UAS–Dfz2 with the high level, ubiquitously expressed E22C–Gal4 driver. (b) The wgPE2 mutant phenotypeand (c) its rescue by overexpression of UAS–Dfz2 with prd–Gal4, which drives high-level expression in odd-numbered segments. No rescue was observed when UAS–fz was overexpressed with either (d)E22C–Gal4 or prd–Gal4 (data not shown). (e) Overexpression of UAS–Dfz2 did not alter the wild-type pattern. (f) The hypomorphic wg pattern was not altered by overexpressing (g)UAS–Dfz2. (h) Maternal and zygotic loss of fz function (fz–) did not alter the wgPE2 mutant phenotype. (i,j) Overexpression of UAS–wgPE2 slightly disrupted denticle pattern and naked cuticle formation (arrow) in (i) wild-type embryos, and rescued denticle diversity in (j) wg null mutants. (k) Co-expression of UAS–wgPE2 with UAS–Dfz2 produced uniform naked cuticle, as does overexpression of wild-type Wg alone in a wg null mutant [3]. (l) Co-expressing UAS–wgPE2 with UAS–fz produced a slight rescue of naked cuticle. Current Biology 2000 10, 1127-1130DOI: (10.1016/S0960-9822(00)00697-7)

Fig. 2 Overexpression of Dfz2 restores molecular response to wgPE2 signaling. (a) Arm is stabilized by wild-type Wg signaling. Stabilization was not observed in (b)wgPE2 mutants, but was restored in odd-numbered segments when (c)prd–Gal4 was used to drive UAS–Dfz2 expression. Arm stabilization was not observed when (d)UAS–fz was overexpressed in wgPE2 mutants, nor when (e)UAS–Dfz2 was overexpressed in hypomorphic wg mutants. (f) Wild-type epidermal cells express En protein in a 2–3-cell-wide stripe in each segment. (g) These stripes were variably narrowed in wgPE2 mutants, and tracheal pit morphology was disrupted (arrow). (h) Both wgPE2 defects were rescued in odd-numbered segments when prd–Gal4 was used to drive UAS–Dfz2 expression. (i) Fz and (j) Dfz2 proteins were detected at roughly equivalent levels when transgenes were overexpressed with prd–Gal4. Current Biology 2000 10, 1127-1130DOI: (10.1016/S0960-9822(00)00697-7)

Fig. 3 Dfz2 and wgPE2 mutants show abnormal Wg protein distribution. (a) Wild-type embryos show a punctate pattern of Wg protein staining over several cell diameters surrounding the wg-expressing row of cells in each segment. Abdominal segments 6 and 7 of stage 10 embryos are shown with anterior to the left. (b) Embryos maternally and zygotically deficient for fz (fz–) showed a wild-type Wg protein distribution, but (c) embryos zygotically deficient for Dfz2 (Dfz2–) showed less punctate staining and high accumulation of Wg surrounding the cells. (d) The wgPE2 mutant protein showed a similar distribution, which (e) was rescued to a more wild-type appearance in odd-numbered segments when Dfz2 was overexpressed with the prd–Gal4 driver. Current Biology 2000 10, 1127-1130DOI: (10.1016/S0960-9822(00)00697-7)

Fig. 4 Altering the level of sugar modification modifies the wgPE2 mutant phenotype. Embryos homozygous for both wgPE2 and (a) a sugarless allele, sgl05007, or (b) a dally allele, dally06464, showed increased naked cuticle compared with wgPE2 single mutants. (c,e) Phenotype of (c) wgPE2 and (e) Df(2)DE mutants. (d,f) Overexpression of dally by inducing expression of the hs–dally transgene (d) worsened the wgPE2 phenotype, but (f) increased naked-cuticle specification in Df(2)DE mutants. (e) No heat shock; (f) heat shock. (g) Overexpressing UAS–Dfz2 with the ubiquitous E22C–Gal4 driver substantially rescued naked cuticle in wgPE2 mutants, but (h) this effect was reversed by co-expressing dally. (g) No heat shock; (h) heat shock. Current Biology 2000 10, 1127-1130DOI: (10.1016/S0960-9822(00)00697-7)