Fig. 4

Paired hyperactivation of neurons with opposing effects on fat storage. a Schematic illustration of parts of the MB circuitry, including neurons, examined. Solid rectangles are dendritic arbors, and solid triangles are axon terminals. Selected MB compartments in α’β’ and γ lobes are indicated. PAMs and MBONs labeled by the drivers used in this paper are indicated. c673a and non-KC Fru neurons are indicated by unconnected yellow boxes. In the diagrams in the other panels, the method of neural hyperactivation is indicated by red color when dTrpA1 is used and orange color when NaChBac1, highlighted on a grey schematic of the MB circuit. b and c Combining hyperactivation of α’β’ KCs with VT30604-GAL4 with hyperactivation of Fru-GAL4 neurons (b) or of c673a-GAL4 neurons (c) results in fat levels that are the same as those in flies in which only α’β’ KCs are hyperactivated, showing the dominant role of α’β’ KC neurons in determining fat content. d and e Combining hyperactivation of MBON-γ5β’2a and MBON-β’2mp with MB011B (d) or of MBON-γ2α’1 with MB077B (e) with hyperactivation of Fru-GAL4 neurons results in suppression of the leanness produced by hyperactivation of Fru-GAL4 neurons alone. Bars indicate means ± SEM, n = 12 samples for pooled controls and n = 4 for other genotypes, as in Fig. 1. Asterisks denote t-test statistical significance: *p < 0.05, **p < 0.005, ***, p < 0.0005. In all experiments, the combined column refers to a single copy of both drivers (GAL4, and split-GAL4) present with a single copy of UAS-NaChBac1 f. A model for fat-regulating MB circuitry. α’β’ KCs regulate both food consumption (via MBONs innervating β’ compartments) and fatty acid synthesis (via MBONs innervating α’ compartments). MBON-γ5β’2a and MBON-γ2α’1 also innervate the γ lobes. γ KC activity affects fatty acid synthesis but not food consumption. The phenotypes shown in Fig. 3 and the epistatic relationships shown in Fig. 4 suggest that the output of the γ KCs that is relevant to fat storage is opposite in sign to that of the α’β’ KCs. However, we do not know the circuits through which γ KCs regulate fat content, so connections from the γ lobes are shown as dotted lines with inhibition bars