2013 Fiscal Year Final Research Report
Neurobiological research of the brain mechanisms controlling insect sexual behavior
| Project/Area Number |
23370035
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Animal physiology/Animal behavior
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| Research Institution | Tokyo Metropolitan University |
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Principal Investigator |
SAKAI Takaomi 首都大学東京, 理工学研究科, 准教授 (50322730)
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| Co-Investigator(Kenkyū-buntansha) |
UENO Kohei 東京都医学総合研究所, 研究員 (40332556)
ASANO Tsunaki 首都大学東京, 理工学研究科, 助教 (40347266)
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| Project Period (FY) |
2011-04-01 – 2014-03-31
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| Keywords | 神経科学 / 昆虫 / 行動学 / 脳・神経 / イメージング |
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| Research Abstract |
The Drosophila painless (pain) gene encodes a transient receptor potentialion channel. First, we identified that pain-reporter is expressed in insulin-producing cells (IPCs) in the adult brain. IPC-specific knockdown of pain expression, ablation of IPCs, and suppression of neurosecretion from IPCs enhance female sexual receptivity. Considering that Pain is a cation channel with Ca2+ permeability, pain knockdown may disturb intracellular Ca2+ signaling in IPCs, leading to defects in the neurosecretion. Thus, we examined whether lack of Drosophila Insulin-like peptides affect female sexual receptivity. In Drosophila, Insulin-like peptide 2, 3 and 5 (Ilp2, Ilp3 and Ilp5) are co-expressed in the IPCs. Females homozygous for Ilp2-, Ilp3-, or Ilp5-knockout (KO) showed hyper sexual receptivity, and targeted expression of Ilp2 RNAi in IPCs phenocopied the phenotype of Ilp2-KO females. Thus, our results suggest that Pain regulates female sexual receptivity through Ilp-secretion.
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[Journal Article] Insulin-producing cells regulate the sexual receptivity through the Painless TRP channel in Drosophila virgin females2014
Author(s)
Sakai, T., Watanabe, K., Ohashi, H., Sato, S., Inami, S., Shimada, N., Kitamoto, T.
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Journal Title
PLoS ONE
Volume: 9(2)
Pages: e88175
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