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Files in this Data Supplement:
Fig. S1. Overexpression of diβ does not affect cell division. (A-C) Confocal images of a third-instar larvae wing disc expressing the chimera diβ (green) in the posterior compartment (p) driven by the engrailed-GAL4 line. (A,B) Staining with an antibody against phosphorylated histone (P-His, red) shows that the expression of diβ does not result in an increase in cell proliferation. (A,C) Cells expressing diβ (green) are visualized using an antibody against the myc epitope present in the chimera; a, anterior.
Fig. S2. Overexpression of diβ does not affect endogenous βPS mRNA levels. (A,B) In situ hybridization of third-instar larvae wing discs expressing the chimera diβ in the posterior compartment (p) driven by the engrailed-GAL4 line. (A) A probe against the extracellular portion of the βPS subunit (βPSext) shows that overexpression of the diβ chimera does not affect transcription of the endogenous βPS. (B) A probe against the cytoplasmic domain of the βPS subunit (βPScyt) shows higher levels of expression in the posterior compartment due to dib overexpression; a, anterior.
Fig. S3. Coexpression of Talin fails to rescue blistering caused by diβ. (A) Expression of diβ in the whole wing pouch using the 638 GAL4 line causes a wing blister phenotype in the adult. (B) Coexpression of Talin fails to completely rescue the blistering phenotype caused by diβ expression. (C) Quantification of the rescue by Talin overexpression using two different GAL4 drivers, 638 and CY2. As a control diβ was also coexpressed with other GAL4 regulated constructs, such as UAS-β-gal.
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