FIGURE 1.

Knock-down of L-type Ca²⁺ channels rescued tau-induced memory defects. (A) Tau expression in the MB (OK107-Gal4) ablated one-hour memory (n = 7 experiments with 50–100 flies each, red bar), as did the expression of an RNAi to the gene encoding the L-type Ca²⁺ channel alpha subunit (Ca-α1D-RNAi, n = 8, blue bar) compared to both Gal4 (n = 12, black bar) and UAS controls (tau, n = 11, open red bars; Ca-α1D-RNAi, n = 9, open blue bars). Co-expression of both transgenes (n = 12, purple bar) resulted in flies with a memory performance equivalent to that of control animals, as did the UAS controls (n = 4, open purple bar). (B) Likewise, expression of tau (n = 9) or Ca-α1D-RNAi (n = 6) in the MB efferent M4/6 neurons (R21D02-Gal4, n = 10) abolished memory. Memory was restored to wild-type levels by co-expression of both transgenes (n = 15). (C) Expression of tau in neuronal subpopulations of the MB impaired memory. Expression was driven in the α′β′ neurons (c305a-Gal4, n = 6 control, n = 4 tau), αβγ neurons (MB247-Gal4, n = 10 control, n = 7 tau) and dorsal paired medial neurons (amn(c316)-Gal4, n = 5 control, n = 4 tau). Data analyzed with Kruskal–Wallis test with Dunn’s post hoc tests (A,C) or with one-way ANOVA with Dunnett’s post hoc tests (B). ^*/#p < 0.05, ^**/##p < 0.01, and ^***/###p < 0.001. Note that UAS/ + controls are the same for each panel.