Extended Data Fig. 7: CREB-downstream genes are required for hypodermal DAF-2 degradation-induced memory.
From: Body-to-brain insulin and Notch signaling regulates memory through neuronal CREB activity
(a) RNAi of unc-43 and unc-73 RNAi worms does not disrupt motility or chemotaxis. Inset images show worms that have successfully migrated from the origin (bottom dot) to the odorant or control spot. (b, c) Chemotaxis Index plots (b) and Learning Index (c) for each condition shown in Fig. 5e. (d) Learning Index at 2 h for control, unc-43, unc-73, or casy-1 RNAi in the neuron-RNAi-sensitized hypodermal DAF-2 AID strain. (e) Additional biological replicates shown for chemotaxis Index plots (top) and Learning Index (bottom) plots for hypodermal DAF-2-AID worms treated with control or unc-43, unc-73, or casy-1 RNAi. (f) Memory was evaluated by calculating the rate of change in CI between the learning indicated time points across replicates. (g) Learning index plot for data shown in Fig. 5f. (h) Naïve index plot for daf-2, daf-2;crh-1, and crh-1 worms. One-way ANOVA, Bonferroni correction. (i) Additional biological replicates shown for daf-2, daf-2;crh-1, and crh-1 memory assays. All biological replicates shown (n = 3). (g, i) Statistical comparisons are shown for daf-2 vs daf-2;crh-1. (b-e, g, i) Two-way ANOVA, Bonferroni post-hoc tests. Mean ± SEM. (f) Two-tailed unpaired t-test. Box plots: center line = median, box range is 25th - 75th percentile; whiskers denote minimum–maximum values. *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001, ****p ≤ 0.0001. All biological replicates are shown. Source data available in supplement.
