Fig. 3.

IDGF3 mutants show defects in clot formation. a Hemolymph preparations were used to detect clot formation using a previously described bead aggregation assay [22]. Idgf3^L1 mutants lacked clot formation visible through a lack of bead aggregation (middle part of the figure underneath the diagram and quantification in the diagram) compared to controls (w¹¹¹⁸). The clotting defect was rescued by ectopic expression of Idgf3 in hemocytes (Idgf3^L1/hml > Idgf3). Data were analyzed using one-way ANOVA and the Tukey test. n.s. = Not significant. ** p < 0.01, *** p < 0.001; error bars represent SEM from 4 independent preparations. b Ubiquitous inducible overexpression of Idgf3 leads to more extensive clot formation measured as thickness of the clot. Control larvae (GT ctr = nontreated genotype control, PR ctr = mifepristone-treated driver control and Control = nontreated driver control) and overexpression larvae (oEx Idgf3) preparations of clots were stained with FITC-conjugated PNA and the thickness of the clots was measured using a confocal microscope. Experimental genotype: w;UAS-Idgf3/Act-Gal4:PR; driver control genotype: w;Act-Gal4:PR/+. The flies were treated 12 h with mifepristone (5 μg/ml) for 12 h. Data were analyzed using one-way ANOVA and the Tukey test. * p < 0.05, ** p < 0.01, *** p < 0.001; error bars represent SEM from 5 independent preparations measured repeatedly at multiple spots of the grid.