Figure 1.

gars^P234KY expression phenocopies plexin mutants and subverts plexin-mediated axonal branching. (A) Schematic of the larval ventral body wall muscles in one hemisegment, showing the transverse nerve (TN), and branches of segmental nerves b (SNb) and d (SNd). The ectopic synaptic contacts often observed on muscles 6 and 7 in gars^P234KY flies are shown in red. (B) In wild-type flies, SNb innervates muscle 12, while the TN entirely bypasses muscles 6, 7, 12 and 13. (C,D) Ectopic axons (arrows) and synaptic contacts can be observed from the SNb and the TN when gars^P234KY is expressed ubiquitously (C) or in muscle (D), phenocopying loss-of-function plexB homozygotes (Carrillo et al., 2010). (E) Ubiquitous (1032-GAL4) and muscle (MHC-GAL4) gars^P234KY expression, but not mutant neuronal (elav-GAL4) or ubiquitous wild-type gars expression, lead to an increased number of ectopic contacts in L3 larvae. This is not seen in a model of spinal muscular atrophy (smn^x7/smn^x7), a second, unrelated neuromuscular condition. Ectopic branches are scored from both the TN and the SNb nerve. (F) Expressing gars^P234KY with a ubiquitous driver in either a plexA or plexB heterozygous knockout background significantly enhances the branching defects from the TN nerve. *P < 0.05, **P < 0.01, Dunn’s multiple comparison test. N.b., gars^P234KY is not expressed in the following flies: control, Smn^x7/Smn^x7, plexA/+, plexB/+, Smn^x7/Smn^x7; plexA/+ and Smn^x7/Smn^x7; plexB/+ (E,F). Scale bars = 10 μm. For all experiments, n > 16 larvae per genotype. Error bars represent ± standard error of the mean (SEM). See also Supplementary Figure S2.