Figure 1

Serotonergic signaling promotes dormancy regulating IIS, whereas octopamine inhibits dormancy. (A) Knocking down the serotonin receptor 5-HT1A in the IPCs strongly reduces dormancy levels (cf. Supplementary Figure S1A), suggesting that serotonin promotes dormancy. (B) Constitutive activation of serotoninergic neurons for 11 days at 12 °C and 16 h:8 h L:D increases ovarian dormancy, confirming that serotonin is a positive regulator of dormancy. Figure 1A and B show percentage dormancy (mean ± binomial SE); assays were performed with 5–7 replicates per genotype, each replicate consisting of ~60 females. ***p < 0.001. (C–F) Expression levels (mean ± standard error [SE]) of dilp2, dilp3, dilp5 in dilp2 > 5-HT1A-RNAi and 4E-BP in dilp2(p) > 5-HT1A-RNAi females at 12 °C as compared to controls. *p < 0.05; **p < 0.01. (G) Downregulation of octopaminergic signaling via OAMB RNAi in the IPCs does not affect dormancy (also see Supplementary Figure S1B). (H) In contrast, however, constitutive activation of octopaminergic neurons decreases dormancy levels. (I) Knockdown of GBR in the IPCs with dilp2-GAL4 has no effect on dormancy (but see Supplementary Figure S1C for a positive yet inconsistent result with dilp2(p)-GAL4). (J) In support of the notion that GABA does not affect dormancy, constitutive activation of GABAergic neurons is ineffective in regulating dormancy. (K) Overexpression of Upd2 in fat body with cg-GAL4, a manipulation that blocks GABA-mediated inhibition of dILP release from the IPCs, does not affect dormancy (also see Supplementary Figure S1D). Shown are the percentage of females in dormancy (mean ± binomial SE); assays were performed with 5–10 replicates per genotype, each replicate consisting of ~50 females. ***p < 0.001.