Figure 9.

Integrated model of calcium signaling transduction in the Drosophila wing disc. (A) Genetic perturbations impacting morphogen and growth pathways result in deviations in agonist (FEX)-stimulated Ca²⁺ signaling responses. Data points of different colors and shapes represent wing discs with various genotypes that are indicated in the legend. Blue-colored, solid data points result in patterning defects and reduced wing growth. Higher Ca²⁺ signaling responses are produced for a given stimulus (15% FEX in all cases). Orange-colored, nonsolid data points result in increased growth. Reduced Ca²⁺ signaling responses are observed for the same stimulus. (B) The parametric plot of the same data set shows increased frequency in Ca²⁺ transients for the growth-suppression perturbations and a decreased frequency for growth-enhancement perturbations. Bloomington stock numbers for UAS-RNAi transgenic lines are included. All the perturbations shown here were driven by the nub > GCaMP6f tester line. (C) An inferred model is shown consistent with observations in (A) and (B). (D) Schematic summarizing key findings from this work and the literature is shown. Both RTK/PLCγ− and GPCR/PLCβ-based signaling contributes to Ca²⁺ activity in vivo and ex vivo (inputs). Perturbations to core Ca²⁺ signaling pathway result in a range of developmental phenotypes (outputs), including wing size, vein differentiation, cell mechanics, and overall tissue shape. To see this figure in color, go online.