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. 2006 Sep-Oct;13(5):659–668. doi: 10.1101/lm.221206

Figure 2.

Figure 2.

Restoring rut in γ MB neurons produces a partial rescue of the learning-deficiency of rut mutants for all odors tested. Three-minute memory for flies carrying GAL4 drivers that express in γ neurons. (A,B,C) Flies bearing H24-GAL4 in combination with the UAS-rut transgene demonstrated significant rescue of rut memory defect over the mutant control group rut2080; H24-GAL4 (P ≤ 0.0006), but were significantly impaired compared to control flies that were CS; H24-GAL4 for all odor combinations tested (P ≤ 0.0006). n = 18 per group except n = 12 for the MCH-BEN experiment. (D,E,F) Flies of the genotype rut2080; NP1131-GAL4; UAS-rut performed significantly better than control flies that were rut2080; NP1131-GAL4 (P ≤ 0.0049), but were significantly impaired compared to control flies that were CS; NP1131-GAL4 for all odor combinations tested (P ≤ 0.0001). n = 18 per group except n = 17 for MCH-BEN experiment. This suggests that driving rut in γ neurons results in partial rescue of the rut learning defect irrespective of odor combination used. In all experiments, the P.I.’s were subjected to a one-way ANOVA with genotype as the main effect, followed by post hoc analysis with the Bonferroni/Dunn test. Statistical significance is indicated by asterisks (**).