Fig. 3
Presynaptic Wnd signaling induces GluR remodeling independently of evoked neurotransmitter release. a Schematic and representative traces of NMJs expressing tetanus toxin in otherwise wild type backgrounds (OK319>TNT: w;OK319-Gal4/+;UAS-TNT/+), in hiw mutants (hiw+OK319>TNT: hiwΔN;OK319-Gal4/+;UAS-TNT/+), and in wnd-OE (wnd-OE+OK319>TNT: w;OK319-Gal4/UAS-wnd;UAS-TNT/+). b Quantification of mEPSP amplitude in the indicated genotypes normalized to OK319>TNT values. Note that reduced mEPSP values persist in hiw and wnd-OE despite the absence of evoked activity. Representative NMJs of the indicated genotypes immunostained (c) and quantified (d) with antibodies against the synaptic vesicle marker vGlut (magenta) and neuronal membrane marker HRP (white). The exuberant synaptic overgrowth characteristic of hiw and wnd-OE also persists in the absence of evoked activity. e Representative images of boutons immunostained with antibodies against the common postsynaptic glutamate receptor subunits GluRIIC and GluRIID. f Quantification of individual GluR puncta intensity normalized to OK319>TNT. Receptor levels in hiw and wnd-OE are reduced despite the absence of evoked activity. Error bars indicate ± SEM. One-way analysis of variance (ANOVA) test was performed, followed by a Tukey’s multiple-comparison test. **p 0.001; ****p 0.0001
