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. 2011 Mar 17;7(3):e1001335. doi: 10.1371/journal.pgen.1001335

Figure 2. Loss-of-function phenotype of krz in the wing.

Figure 2

(A) Wild type control wing. (B) 638-Gal4/+; UAS-FLP/+; FRT82 Df(3R)krz/FRT82 M(3)w. In this genotype all wing cells are homozygous for the Df(3R)krz, and the wings show reduced size and incorrect folding. (C) UAS-dicer/+; nub-Gal4/+; UAS-ikrz/+. In this genotype krz iRNA is expressed in the entire wing pouch, and the wing is very similar to that shown in B. (D) wor-Gal4/UAS-krz; krz1/Df(3R)krz. The expression of krz in the CNS driven by wor-Gal4 rescues the lethality of the krz1/Df(3R)krz combination, and the wings develop without krz expression. (E) Third instar wing disc of krz1/Df(3R)krz genotype, showing a reduced size and the expression of activated-Cas3 (green) throughout the disc. (F) Third instar wing disc of wor-Gal4/UAS-krz; krz1/Df(3R)krz genotype, showing a normal expression of Smo (red) and the rescue of wing disc size. (G–H) Genetic interaction between Notch and Krz. The reduction in Notch expression (638-Gal4/+; UAS-iNotch/+; G) causes the thickening of the wing veins and the elimination of the wing margin (G). This phenotype is augmented when the expression of krz is also reduced (638-Gal4/+; UAS-iNotch/UAS-ikrz; H). (I–J) Genetic interaction between EGFR and Krz. The reduction in EGFR activity (638-Gal4/+; UAS-EGFRDN/+; I) causes the loss of veins and a reduction in wing size (I). This phenotype is not modified when the expression of krz is also reduced (638-Gal4/+; UAS-EGFRDN/UAS-ikrz; H). (K–L) Genetic interaction between Hh and Krz. The reduction in Hh expression (638-Gal4/+; UAS-ihh/+; I) causes a reduction in wing size and in the distance between the veins L3 and L4 (K). This phenotype is not modified when the expression of krz is also reduced (638-Gal4/+; UAS-ihh/UAS-ikrz; L).