Fig. 5
Glutamate spillover induces repetitive reversals by presynaptic activation of MGL-2. a mgl-2 mutation ameliorates increased repetitive reversals of glt-1 mutants. The effect is reversed by re-expression of MGL-2 specifically in RIM neurons (Kruskal−Wallis ANOVA with Dunn’s multiple comparison test, n.s., nonsignificant, ***p < 0.0005, *p < 0.05; WT, black circles, n = 30, mgl-2(tm355), black boxes, n = 13, tdc-1pro::MGL-2, black triangles, n = 25, glt-1(ok206), open circles, n = 21, glt-1(ok206); mgl-2(tm355), open boxes, n = 24, glt-1(ok206); mgl-2(tm355); tdc-1pro::MGL-2, open triangles, n = 25 movies). b MGL-2 expression in AIB neurons rescues repetitive reversals (WT, black circles, n = 21, glt-1(ok206), black boxes, n = 21, glt-1(ok206); mgl-2(tm355), black triangles, n = 22, glt-1(ok206); mgl-2(tm355); inx-1pro::MGL-2, open triangles, n = 10 movies). c Channelrhodopsin activation of RIM promotes GLT-1-mediated repetitive reversals (WT, black circles, n = 11, glt-1(ok206), black boxes, n = 12, glt-1(ok206); mgl-2(tm355), black triangles, n = 10 movies). a–c Bars, mean ± SEM. b, c ANOVA Tukey’s HSD post hoc test, ***p < 0.0005, *p < 0.05. In (c), while not significant at the level of p < 0.05, the trend towards fewer repetitive events in animals also lacking mgl-2 is consistent with our observations in (a, b). d GFP-tagged MGL-2 localizes to RIM neurite (left), but not to mCherry-labeled synapses (middle); merge (right). Scale bar, 5 μm; nerve-ring region is indicated with dotted line; 2-μm-thick sum intensity projections. Source data are provided as a Source Data file
