Figure 5.

SAP47 knockdown. A, Western blot of WT and white mutants. Given that all strains are in the w¹¹¹⁸ mutant background (see Materials and Methods), a test of SAP47 expression in w¹¹¹⁸ is warranted, which shows no difference in SAP47 expression to WT. Antibodies used are the monoclonal nc46 for SAP47 detection and, as loading control, the monoclonal ab49, the latter labeling CSP, another presynaptic protein. A′, white mutants are not impaired in associative function. WT and w¹¹¹⁸ perform equally well in the associative learning paradigm. The PREF scores underlying PI values are documented in supplemental Figure 3 (available at www.jneurosci.org as supplemental material). N = 16, 16. Shared lettering above plots signifies p > 0.05 in a Mann–Whitney U test. B, Western blot of SAP47 knockdown. The elav-Gal4 driver-control and the UAS-RNAi-SAP47 effector-control strains show no difference to WT in terms of SAP47 expression level, but the knockdown larvae show an obvious reduction. B′, SAP47 knockdown larvae are impaired in associative function. Associative function is reduced to ∼50% of control levels upon expression of an RNA-interference mRNA, using elav-Gal4 as driver- and UAS-RNAi-SAP47 as effector-strain. Both controls perform equally well (see supplemental Fig. 8A, available at www.jneurosci.org as supplemental material) and are therefore pooled. Notably, this RNAi-induced reduction of associative function is as severe as the one seen upon a total lack of SAP47 in the Sap47¹⁵⁶ mutant (Fig. 2). The PREF scores underlying the PI values are documented in supplemental Figure 4 (available at www.jneurosci.org as supplemental material). N = 32, 19, 36. Different lettering above plots signifies p < 0.05/2 in Mann–Whitney U tests.