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. 2014 May 19;9(5):e97692. doi: 10.1371/journal.pone.0097692

Figure 6. Arp2 and Arp3 loss-of-function mirror the defects in NMJ development observed upon abp1 deficiency.

Figure 6

(A) The immobilized SH3 domain of Abp1 (GST-SH3) specifically precipitates endogenous WASP and Scar from fly head extracts whereas GST and a point-mutated SH3 domain (GST-SH3*; P523A mutation), respectively, do not. (B) Model depicting that Abp1 interfaces with both WASP and Scar and may regulate Arp2/3 complex dependent actin dynamics at the NMJ using both Arp2/3 complex activation pathways. (C) NMJs at muscles 6/7 of abdominal segment A2 of wt, Arp2 RNAi #1, Arp2 RNAi #2 and Arp3 RNAi expressing larvae stained with HRP (green) and anti-Dlg (red). (D,E) Quantitative analyses of type Ib boutons and of terminal axonal branch points visualize that Arp2/3 complex deficiency phenocopies abp1 knock-out in reducing type Ib bouton number and terminal branch points of the axon within NMJs. (F,G) Quantitative analyses revealing that larvae with presynaptic Arp2 RNAi #2 or Arp3 RNAi phenotypically mirror presynaptic Abp1 RNAi, as specifically type Ib bouton formation but not the formation of terminal axonal branch points is affected. Data represent mean±SEM. n = 18–36/genotype. * = p<0.05, ** = p<0.01 and *** = p<0.001. One way ANOVA post Tukey.