Fig. 5: FMRP and Draper genetically interact to drive central PDF-Tri neuron elimination.

a Whole brains (5 DPE) labeled with anti-PDF in all controls (top row); genetic background control (w¹¹¹⁸), dfmr1 null heterozygote control (w¹¹¹⁸; dfmr1^50M/+), and draper null heterozygote control (w¹¹¹⁸; draper^∆5/+). All three controls lack the central brain PDF-Tri neurons. The bottom row shows the three experimental genetic conditions; the dfmr1 homozygous null mutant (w¹¹¹⁸; dfmr1^50M), the draper homozygous null mutant (w¹¹¹⁸; draper^∆5), and the dfmr1/draper null trans-heterozygote (w¹¹¹⁸; dfmr1^50M/draper^∆5). All three genotypes exhibit persistent PDF-Tri neurons (arrows). Scale bar: 50 μm. Images are representative of three independent experiments. b Quantification of anti-PDF area for the central PDF-Tri neurons in all six genotypes. Kruskal–Wallis followed by Dunn’s multiple comparison test, p > 0.9999, 94.75 ± 25.94 n = 25 control, 25.60 ± 7.212 n = 19 draper^Δ5/+, 66.16 ± 19.78 n = 19 dfmr1^50M/+, p = 0.0068 94.75 ± 25.94 n = 25 control vs. 417.2 ± 84.86 n = 20 dfmr1, p < 0.0001 94.75 ± 25.94 n = 25 control vs. 553.2 ± 69.81 n = 16 draper, p = 0.0020, 94.75 ± 25.94 n = 25 control, 438 ± 69.81 n = 31 dfmr1/draper. c Quantification of anti-PDF puncta number for the central PDF-Tri neurons in all six genotypes. Kruskal–Wallis followed by Dunn’s multiple comparison test, p > 0.9999, 15.15 ± 3.3 n = 27 control, 8.091 ± 1.931 n = 22 draper^Δ5/+, 9.667 ± 3.067 n = 18 dfmr1^50M/+, p = 0.176 15.15 ± 3.3 n = 27 control vs. 30.65 ± 4.944 n = 18 dfmr1, p = 0.0003 15.15 ± 3.3 n = 27 control vs. 45.81 ± 5.443 n = 16 draper, p = 0.0155, 15.15 ± 3.3 n = 27 control, 32.68 ± 4.069 n = 31 dfmr1/draper. The scatter plot graphs show mean ± SEM. Sample size is n = number of animals. Significance shown for p > 0.05 (not significant, N.S.), p < 0.05 (*), p < 0.01 (**), and p < 0.001 (***). Source data for this figure are provided in Source Data file.