Figure 1.

Mutants of white have a defect in acquisition that can be rescued by white⁺ and mini-white transgenes. (a) Olfactory learning acquisition curves are shown for w¹¹¹⁸ mutants and wildtype Canton-S (w⁺). The w¹¹¹⁸ mutant has lower associative STM with one and three shock pairings to odor (two-way ANOVA, Adj. R² = 0.475, F_6,121 = 20.157, p < 0.0001, n = 10–13; Tukey post hoc w⁺ versus w¹¹¹⁸, p < 0.05, n = 64); (b) one-trial olfactory learning for wildtype and the w^coral, w^apricot, and w¹¹¹⁸ mutants are shown. Representative photos of the heads are provided above the graph to demonstrate the level of white activity remaining in eye pigment cells for each mutant. All mutants were equally poor in associative STM and significantly different from wildtype (ANOVA, Adj. R² = 0.321, F_3,32 = 6.524, p < 0.001, n = 9); (c) poor one-trial learning for w¹¹¹⁸ was rescued by a genomic duplication (w¹¹¹⁸; Dp(1;3)DC050- wDup; ANOVA, Adj. R² = 0.356, F_2,27 = 9.022, p < 0.001; Tukey post hoc, p < 0.05; n = 10); (d) poor one-trial learning for w¹¹¹⁸ was rescued by two mini-white marked GAL4 drivers (ANOVA, Adj. R² = 0.254, F_2,25 = 5.590, p < 0.01; Tukey post hoc, p < 0.05; n = 8–10). In panels b, c, and d, groups that do not share letters above the box plots are significantly different from each other according to the Tukey post hoc test (* p < 0.05).