Fig. 2

abi controls synaptic structure and function at the neuromuscular junction (NMJ). a Loss of Abi causes synaptic overgrowth with excessive satellite bouton formation. Sample confocal images of anti-HRP labeled NMJs 6/7 and 4 in wild type, abi⁵/Df, and C155-GAL4/+; UAS-HA-abi,Df/abi⁵ (Abi rescue-pre). Insets (left panels) show higher magnification views of boutons marked by white asterisks. Satellite boutons are indicated by arrowheads. Scale bars: 20 μm. b Quantification of total bouton number normalized to muscle surface area ([#/μm²] × 10³; top) and satellite bouton number (bottom) at NMJ 6/7 in wild type, abi⁵/+, Df/+, abi⁵/Df, C155-GAL4/+; UAS-HA-abi,Df/abi⁵ (Abi rescue-pre), C155-GAL4/+; UAS-HA-abi^Δ30–65/+; abi⁵/Df (AbiΔ30–65 rescue-pre), C155-GAL4/+; UAS-HA-abi^Δ123–175,Df/abi⁵ (AbiΔ123–175 rescue-pre), C155-GAL4/+; UAS-HA-abi^W452K,Df/abi⁵ (Abi-W452K rescue-pre), C155-GAL4/+; UAS-HA-abi^4YE,Df/abi⁵ (Abi-4YE rescue-pre), C155-GAL4/+; UAS-HA-abi^4YF,Df/abi⁵ (Abi-4YF rescue-pre), 24B-GAL4,abi⁵/UAS-HA-abi,Df (Abi rescue-post). c, d Loss of Abi causes an increase in NMJ synaptic transmission. c Representative two-electrode voltage-clamp (−60 mV) records from muscle 6 with 0.5 Hz nerve stimulation. Sample excitatory junction current (EJC) traces are shown for wild type, abi⁵/Df, abi-GAL4/+ transgenic control, and abi-GAL4/+; UAS-HA-abi,Df/abi⁵ (abi-GAL4 rescue). d Quantification of EJC amplitude. e Schematic view of the domain structure of wild-type Abi and Abi variants used in rescue experiments. WAB, WAVE-binding domain; HHR, homeodomain homologous region; P, proline-rich region; SH3, Src homology 3 domain. Point mutations are indicated by stars. Bar graphs show mean ± s.e.m. Sample number analyzed is indicated inside bars. Statistical analyses were performed by one-way analysis of variance with Tukey–Kramer post hoc test. Comparisons are with wild type (*P < 0.001; **P < 0.01; ***P < 0.05)