Fig. 5: ACC inhibition in cortex glia rescues the memory impairment induced by defective Dh44 signalling.
a The dual Dh44-R1 and ACC KD in cortex glia rescued the memory deficit observed upon the single KD of Dh44-R1 (n = 12, F4,55 = 14.53, p = 4 × 10−8). b Single-cycle training elicited a faster pyruvate accumulation in MB neuron axons following azide application (5 mM) as compared to non-associative unpaired conditioning (n = 12, t22 = 2.07, p = 0.04). This effect was lost in the single Dh44-R1 knockdown condition (n = 12, t22 = 0.96, p = 0.34), but rescued upon dual Dh44-R1 and ACC KD in adult cortex glia (n = 12, t22 = 2.12, p = 0.04). c A combination of two GAL4 drivers was used to target both MP1 neurons and cortex glia at the adult stage. As expected, Dh44 KD in both MP1 neurons and cortex glia caused a memory defect, which was rescued in the condition of dual Dh44 and ACC KD (n = 13, F4,62 = 5.29, p = 0.001). RNAi lines KK108591 (Dh44-R1, panel A), JF03208 (Dh44-R1, panel B), GD3482 (ACC) and JF01822 (Dh44) were used in this figure. Data are represented as mean ± SEM. ns: not significant, p > 0.05, *p < 0.05, **p < 0.01, ****p < 0.0001 by two-tailed Student’s t test (b) or Tukey’s pairwise comparison following one-way ANOVA (a, c). Source data are provided as a Source Data file.
