Figure 4

DFsn is required for normal synaptic function. (a) Representative traces of evoked and spontaneous transmitter release recorded from wild-type (WT), DFsn^f06595/Df [P(f06595)/Df(2R)7872], DFsn^f06595/Df-Res [presynaptic rescue: P(f06595)/Df(2R)7872; elav Gal4/UAS-HM-DFsn] and DFsnf06595/Df; wnd¹/wnd³ third instar larvae. (b-e) The mean mEJP amplitude (b), EJP amplitude (c) and quantal content (d) are plotted for WT, DFsn^f06595/Df, DFsn^f06595/Df-Res and DFsnf06595/Df; wnd¹/wnd³ (n = 13, 15, 10 and 9 cells, respectively). The DFsn^f06595/Df mutant shows reduced EJP amplitude and reduced quantal content (p < 0.001 for DFsn^f06595/Df versus WT). These electrophysiological defects in the DFsn^f06595/Df mutant are all rescued by presynaptic expression of DFsn (p < 0.001 for DFsn^f06595/Df-Res versus DFsn^f06595/Df;p > 0.5 for DFsn^f06595/Df-Res versus WT). wallenda suppresses the reduction of mini frequency in the DFsn^f06595/Df mutant (p > 0.5 for DFsn^f06595/Df; wnd¹/wnd³ versus WT). The EJP amplitude and the quantal content of the double mutant DFsnf06595/Df; wnd¹/wnd³ are not significantly different than DFsn^f06595/Df (p > 0.1), demonstrating that wallenda does not suppress the DFsn^f06595/Df defect in evoked release.