Fig. 7
From: Genetic background mutations drive neural circuit hyperconnectivity in a fragile X syndrome model
GFI synaptic projections dependent on dfmr150M background mutations. a Giant fiber interneuron (GFI) TRITC-dextran dye injected (magenta) in the indicated genotypes; genetic background control (w1118), genomic rescue (dfmr1.14/+; dfmr150M), dfmr150M heterozygote (dfmr150M/+), homozygous null mutant (dfmr150M), independent dfmr1 null (dfmr1B55), and second independent dfmr1 null over a deficiency (dfmr12/Df). FMRP was also removed using RNAi driven by the ubiquitous daughterless Gal4 driver (UH1; UH1>dfmr1 RNAi2). Arrows indicate projections. Scale bar, 10 μm. b Western blot of FMRP levels in w1118, dfmr150M/+, dfmr150M, and dfmr1B55 (top); and w1118, dfmr150M, elav>dfmr1 RNAi1 and UH1>dfmr1 RNAi2 (bottom). FMRP bands are labeled in green and α-Tubulin loading controls in magenta. c Quantification of projections in w1118 (n = 20), dfmr150M (n = 18), and the dfmr1 rescue condition (n = 22). d Quantification of projections in w1118 (n = 13), dfmr150M/+ (n = 13), dfmr150M (n = 10), and dfmr1B55 (n = 12). e Quantification of projections in w1118 (n = 9), dfmr150M (n = 9), and dfmr12/Df (n = 10). f Quantification of projections in UH1/+ control (n = 17) and UH1>dfmr1 RNAi2 (n = 16). Each gray dot represents the projection number for an axon bend in one animal. The black dot represents the mean and red bars represent the standard error of the mean
