Figure 4. APPL inhibits FASII function in R3 neurons.

(A) The memory deficit of hemizygous FasII^e76 mutants can be rescued by FASII expression in R3 neurons, but not by the UAS-FASII transgene alone.

(B) An RNAi mediated knock-down of FASII in R3 neuron also results in memory deficit.

(C–D) Knock-down of FasII in R3 neurons leads to a 38% reduction of FASII levels. Rectangles indicate regions in which the means of gray value were determined to calculate the quotients of R3/R2 intensities (n = 6; p = <0.001; t-test; mean intensity ratio R3/R2: WT: 0.828 ± 0.1107; RNAi: 0.517 ± 0.0507).

(E) Heterozygosity for Appl or FasII suppresses memory deficits of homozygous FasII^e76 or Appl^d mutants, respectively.

(F) Knock-down of FasII in R3 neurons suppresses memory deficit in Appl^d mutants.

(G) 189Y-GAL4 driven overexpression of FASII or APPL alone reduces the working memory, but when both were co-expressed they suppress the memory deficit of each other.

(H) Overexpression of sdAPPL does not affect memory but does suppress the FASII overexpression phenotype.

(I) sAPPL^Long does neither affect the memory nor suppress the FASII overexpression phenotype.

(J) Overexpression of sAPPl^Short abolishes the memory and prevents the FASII induced phenotype.

The 189Y-GAL4 driver was used in all experiments; n = 25 males for all groups, except in (E) n = 16–25 females; age 3–5d; Kruskal-Wallis ANOVA, Bonferroni post-hoc. See Data S4 for statistical analysis and Figure S4 for FASII expression analysis in all types of ring neurons.