Figure 7.
Integrating cVA and taste is key to controlling female receptivity
(A) Top: EM reconstruction of labellar GRNs (lGRN, green) and G2N-SLP1 (yellow) in FAFB. Middle: EM reconstruction of aSP-g neurons in FAFB, right hemisphere: purple, left hemisphere: gray. Bottom: confocal image of aSP-g neurons in a female brain, reporter expression driven by aSP-g-SS1/SS2, maximum projection. Scale bars, 20 μm.
(B) Schematic connectivity of aSP-g input pathways based on FAFB and the hemibrain. Number of synaptic connections: lGRN-G2N-SLP1: 63; G2N-SLP1-aSP-g: 139; ORN-lPN: 8,764; lPN-aSP-g: 81.
(C) Confocal image of Ir94e labellar GRNs in a female brain, reporter expression driven by Ir94e-GAL41, maximum projection. Scale bars, 20 μm.
(D) Ir94e GRNs respond strongest to compounds on male genitals. Normalized GCaMP7f mean responses to labellar presentation of stimuli. Horizontal bars show the population mean of 10 flies, single trials.
(E) Ir94e GRNs GCaMP7f responses, average responses from 10 flies. Black bars: labellar stimulation. Shaded area is SEM.
(F) Pulsed optogenetic activation of both cVA olfactory and Ir94e gustatory PNs simultaneously increases female receptivity, while individual activation does not. Activating DA1 lPN-SS alone (orange), IR94e GAL4 alone (green), or both (blue) in females paired with wild-type males, compared with controls (black, gray).
(G and H) Manipulating aSP-g in virgin females paired with wild-type males. (G) Constant optogenetic activation of aSP-g-SS1/SS2 increased female receptivity. (H) Using Kir2.1 to block aSP-g-FLP1 or aSP-g-FLP2 decreased female receptivity.
(I) Constant optogenetic activation of aSP-g-SS1/SS2 in female pairs in the light increased female-female aggression. Boxplot and hinges represent median and first and third quartiles.
(J) Alternative interactions between aSP-g and pC1 neurons: in a parallel architecture, both populations control receptivity independently, and activating aSP-g while ablating pC1 could increase receptivity, compared with no activation. In a serial architecture, aSP-g effect on receptivity depends on intact pC1, and their activation cannot overcome pC1 ablation.
(K) Behavioral epistasis: optogenetic activation of aSP-g while pC1 neurons are ablated. Constant optogenetic activation of aSP-g in females either alone (purple) or while pC1-SS neurons were ablated (black). aSP-g activation increased female receptivity, compared with genetic control (gray), and activating aSP-g while pC1 neurons are ablated partially rescued the receptivity impairment of pC1-ablated females (yellow).
(L) Feature separation model of an olfactory stimulus. cVA signal diverges into two parallel second-order pathways; third-order neurons represent distinct cVA-related scenarios by specific response kinetics and the integration of signals from other sensory modalities. d, distance; θ, angular direction; v, speed.
See also Figure S7.