erect wing integrates cellular signaling to regulate synaptic growth. (a-d) Genetic interaction of ewg with known signaling pathways in synaptic growth regulation. Synaptic growth was analyzed at third instar NMJs by quantifying type 1b boutons at muscle 13 of ewgl1eFeG clones (white bars and '-' at the bottom of the column) or of ewgl1eFeG clones in the presence of an ewg wild-type copy (grey bars and '+' at the bottom of the column) in combination with either transgenes for UAS constructs or transheterozygous combinations of mutant alleles (witA12/witB11) as described for Figure 1. Wild type (bar 1), ewg loss of function (LOF, bar 2) and ewg gain of function (GOF, black bars, bar 3) were compared to LOF and GOF mutants in Notch (a), Wingless (b), AP-1 (c) and TGF-β/BMP (d) pathways. Overexpression of N is shown in the presence of both ewg copies ('++' at the bottom of the column), as one ewg copy in the presence of excess N does not result in a significant increase of bouton numbers compared to wild type. For both N and tkvA, two copies of UAS transgenes were used; a single copy did not significantly alter bouton numbers. Shown are means of bouton numbers with standard errors (n = 11-23, numbers at the bottom of bars). Bars are numbered below the x-axis. Statistical significance of differences from comparisons with wild type is shown on top of bars (***p < 0.0001, ** p < 0.005, n.s. for non significant). Other relevant comparisons are marked by horizontal bars with the statistical significance indicated on the side.