Supplementary Figure 6: Ectopic wingless signalling induced by Axin cancer-mutant expression in Drosophila wing discs is rescued by aggregon mutation.

Related to Figure 6. (a) Schematic presentation of gene targeting strategy to generate Axin knock-in flies. (b) Confirmation of genetic modification of Axin knock-out mutant flies. (c) Quantification of the average clone size of the P compartment occupied by GFP-positive tissue in different genotype (n = 5). Error bars represent SDs. *** p<0.0001. (d) Excess Wingless (Wnt) signalling in DAxin-V72R clones is rescued by aggregon mutation. Larvae were grown at 29°C. In GFP-negative cells, the indicated DAxin variants were knocked in the endogenous axn locus. Expression of the Wg target genes senseless (Sens) and distalless (Dll) was analysed using immunostaining. DAxin-V72R-expressing clones overgrow the posterior tissue (arrowheads) and show ectopic expression of both Sens and Dll. Wg target gene expression by the V72R cancer mutant is rescued by introduction of the secondary aggregon mutation I169R L170R. Boundary between anterior and posterior tissue in wing discs is marked by a dotted line. Scale bar 100 µm (e) Mutation of the region homologous to the human RGS aggregon does not rescue DAxin-V72R suppressor activity. In shown mosaic posterior compartments, the V72R Y86R F87R DAxin variant (homologue of human Axin suppressor mutant L106R F119R W118R) was knocked in the endogenous axn locus in GFP-negative cells. Mutant clones overgrow the posterior tissue at all temperatures tested.