Abstract
In a variety of animal species, females hold a leading position in evaluating potential mating partners. The decision of virgin females to accept or reject a courting male is one of the most critical steps for mating success. In the fruitfly Drosophila melanogaster, however, the molecular and neuronal mechanisms underlying female receptivity are still poorly understood, particularly for virgin females. The Drosophila painless (pain) gene encodes a transient receptor potential (TRP) ion channel. We previously demonstrated that mutations in pain significantly enhance the sexual receptivity of virgin females and that pain expression in painGAL4-positive neurons is necessary and sufficient for pain-mediated regulation of the virgin receptivity. Among the painGAL4-positive neurons in the adult female brain, here we have found that insulin-producing cells (IPCs), a neuronal subset in the pars intercerebralis, are essential in virgin females for the regulation of sexual receptivity through Pain TRP channels. IPC-specific knockdown of pain expression or IPC ablation strongly enhanced female sexual receptivity as was observed in pain mutant females. When pain expression or neuronal activity was conditionally suppressed in adult IPCs, female sexual receptivity was similarly enhanced. Furthermore, both pain mutations and the conditional knockdown of pain expression in IPCs depressed female rejection behaviors toward courting males. Taken together, our results indicate that the Pain TRP channel in IPCs plays an important role in controlling the sexual receptivity of Drosophila virgin females by positively regulating female rejection behaviors during courtship.
Highlights
To understand how sexual behavior is controlled by the nervous system, it is essential to identify the relevant neural circuits in the brain and elucidate how they integrate multiple sensory cues to regulate highly coordinated motor outputs
Our results demonstrate that insulin-producing cells (IPCs) in the pars intercerebralis (PI) are critical for the Pain-mediated regulation of female sexual receptivity and that neurosecretion from IPCs negatively controls the sexual receptivity of virgin females by positively regulating their rejection responses toward courting males
No significant difference was detected between wild-type and pain2 females in the courtship latency (Figure 1E), courtship index (Figure 1F), and general locomotion (Figure S1). These results indicate that pain2 and wild-type females elicit male courtship behavior at a similar level and that the rapid copulation of virgin pain2 females is due to their enhanced sexual receptivity, as was observed for pain1, pain3, and painGAL4 females
Summary
To understand how sexual behavior is controlled by the nervous system, it is essential to identify the relevant neural circuits in the brain and elucidate how they integrate multiple sensory cues to regulate highly coordinated motor outputs. Considering that males court wild-type and pain females to the same extent, the enhanced mating success of pain females is most likely to be caused by increased female sexual receptivity. The enhanced female receptivity in pain mutants is rescued and phenocopied, respectively, by expressing the wild-type pain gene and pain RNAi using painGAL4. The expression of pain in painGAL4-positive neurons is necessary and sufficient for the Pain-mediated regulation of female sexual receptivity [20]. PainGAL4 drives GFP reporter gene expression in various brain regions including the mushroom bodies (MBs), a part of the central complex (CX), and the pars intercerebralis (PI). PainGAL4-positive brain regions could mimic the phenotype of pain mutant females and enhance their sexual receptivity. Our results demonstrate that insulin-producing cells (IPCs) in the PI are critical for the Pain-mediated regulation of female sexual receptivity and that neurosecretion from IPCs negatively controls the sexual receptivity of virgin females by positively regulating their rejection responses toward courting males
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
