Fig 1. MIP receptor signaling promotes short-term gustatory plasticity.

(A) Overview of the gustatory plasticity assay: Short-term conditioning with NaCl in the absence of food induces aversive learning, known as gustatory plasticity [11,12]. Synchronized young adult C. elegans are washed in buffer in the absence of food with salt (NaCl-conditioned) or without NaCl (mock-conditioned). Chemotaxis behavior to NaCl is then tested on a quadrant plate. After ten minutes, a chemotaxis index (CI) is calculated as indicated. (B-C) Gustatory plasticity of sprr mutants. Individual CIs are plotted as blue dots. Boxplots indicate 25^th (lower boundary), 50^th (line), and 75^th (upper boundary) percentiles. Whiskers show the minimum and maximum values. Outliers are indicated as black dots. (B) Comparison of CIs for mock-conditioned animals yielded p>0.05 for all genotypes (not indicated on graph). NaCl-conditioned mutants of sprr-1 and sprr-3 displayed wild-type avoidance of NaCl, whereas the response of sprr-2 was significantly reduced. Data were analyzed by one-way ANOVA and Tukey post-hoc test (n ≥ 4). (C) The MIP receptor gene sprr-2 is required for gustatory plasticity. Expression of sprr-2 cDNA under the control of its promoter sequence [sprr-2p::sprr-2] rescues the plasticity defect of NaCl-conditioned sprr-2 mutant animals. Statistical comparisons by one-way ANOVA and Tukey post-hoc test (n ≥ 12). *p<0.05; ***p<0.001; n.s., not significant. See also S1 and S2 Figs.