動物維持生理的恆定現象有賴於內分泌系統和神經系統來共同運作,研究證實當果蠅的wide awake (即wake;生合成WAKE)在胰島素生成細胞(insulin producing cells; IPCs)中的表現缺乏,將影響該細胞GABAA receptor (Resistance to dieldrin; Rdl)的功能而促進類胰島素胜肽(insulin-like peptides; Ilps)的分泌,進而透過胰島素/類胰島素生長因子訊息(insulin/insulin-like growth factor signaling; IIS)將促使咽側腺 (corpora allata; CA)合成青春激素(Juvenile hormone; JH)並使得20-羥基蛻皮酮(20-hydroxyecdysone; 20E)的水平降低,證據顯示,這些失衡的內分泌訊號均能直接影響嗅覺感覺神經元(olfactory sensory neurons; OSNs)調控雄果蠅同性間的求偶行為發生。本文進一步釐清這些彼此冗餘的內分泌訊息(redundant signaling pathways)在嗅覺感覺神經元中也可能相互協同合作維持該細胞內分泌訊息網絡的恆定。證據顯示,若嗅覺感覺神經元中的IIS增強可能抑制shade的表現,而該基因所表現的 20-hydroxylase 作用於蛻皮激素(ecdysone)轉化為具生物活性啟動蛻皮激素訊號的20E配體(ligand),因此胰島素訊號IIS可能下調該細胞的蛻皮激素訊號;此外,蛻皮激素訊號可能參與調節let-7 microRNA (miRNA)的表現,若蛻皮激素訊號受IIS而下調將使得let-7 microRNA的表現降低,初步推斷let-7 miRNA可能調控青春激素訊號所活化表現的初始反應基因Krüppel homolog 1 (Kr-h1)的表現,因此下調蛻皮激素訊號也可能在嗅覺感覺神經元中參與維持青春激素訊號初始反應基因的表現。綜合上述的結果,胰島素訊號、蛻皮激素訊號及青春激素訊號這三種不同的內分泌訊息在嗅覺感覺神經元中相互協同形成一個內分訊息網絡,當其中特定的內分泌訊息失衡將可能影響該細胞中其他的內分泌訊息,終致發生非常規的雄性間求偶行為反應發生。
The nervous and endocrine systems coordinate with each other, closely affecting the physiological and behavioural responses of animals. Evidence shows that a deficiency of wide awake (also known as wake, encoding WAKE) in insulin-producing cells of Drosophila melanogaster modulates the GABAA receptor (Resistance to dieldrin; Rdl), thereby promoting secretion of insulin-like peptides. Insulin/insulin-like growth factor signalling (IIS) stimulates juvenile hormone synthesis in corpus allata (CA) and leads to a considerable decrease in 20-hydroxyecdysone levels. Finally, due to a reduction in ecdysone signalling and enhancement of IIS and JH signalling, targets on the specific olfactory sensory neurons (OSNs) that prompts male-male courtship alone. Further evidence from this study, these redundant endocrines signaling pathways still cooperate with each other in the specific OSNs for male-male courtship inhibition. This is a long course involving multiple molecular interactions which in turn give rise to an intricate network in the organism, because neuro-endocrine networks imbalances influence specific OSNs, which ultimately results in unconventional behavioural responses.