Fig. 4

Abi pathway restrains synaptic development by inhibiting bone morphogenetic protein (BMP) signaling. a, b Loss of Abi, Abl, and Rac1-SCAR components increases P-Mad in motor neurons. a Single confocal sections of neuromuscular junction (NMJ) 6/7 (top) and ventral nerve cord (VNC) co-labeled with anti-P-Mad and anti-HRP (NMJ) or anti-Even Skipped (Eve; VNC) shown for wild type, abi⁵/Df, Abl¹/Abl⁴, C155-GAL4/+, and C155-GAL4/+; UAS-Rac1^T17N/+. b Quantification of P-Mad intensity normalized to HRP or Eve in the indicated genotypes. c, d Synaptic overgrowth induced by loss of Abi, Abl, or presynaptic Rac1 depends on BMP signaling. c Sample confocal images of anti-HRP-labeled NMJs in wild type, abi⁵/Df, wit^A12/+, wit^A12,abi⁵/+,Df, wit^A12/wit^B11, and wit^A12,abi⁵/wit^B11,Df. d Quantification of synaptic structure at NMJ 6/7 in the indicated genotypes. Bar graphs indicate mean ± s.e.m. The number of NMJ branches (b, upper panel), Eve-positive motor neurons (b, bottom panel), or NMJs (d) analyzed for each genotype is indicated inside bars. All comparisons are with wild type (b, d) unless indicated (one-way analysis of variance with Tukey–Kramer post hoc test; *P < 0.001; n.s. not significant). Scale bars: a, 2 μm (NMJ); a, 5 μm (VNC); c, 20 μm