Estrogen can regulate oxytocin receptor expression, which is mediated through estrogen receptors (ESRs) in mammals, initiating parturition. To further study the reproductive physiological process of ovoviviparous teleosts, guppies (Poecilia reticulata) were employed as the research model in the present study to identify the transcriptional regulation of ESRs on isotocin receptors (itrs). Since guppy embryos develop inside the ovary, in the present study, the levels of itrs in the ovarian stroma of pregnant female guppies treated with estradiol (E₂) in vitro were tested. E₂ increased only itr2 mRNA levels 3 h post-treatment, with no variation in itr1 mRNA expression levels. In vivo, pregnant guppies were immersed in different concentrations of E₂, significantly increasing the relative expression levels of itr1 and itr2 in the ovary. Moreover, based on dual-fluorescence in situ hybridization (ISH), both esrs and itrs mRNAs were localized in the same cells around the embryos in the ovary. To further investigate the regulation of itr transcription by estrogen, a luciferase reporter assay was performed, and the results demonstrated that E₂ treatment could induce E₂-dependent repression of luciferase activity in cells transfected with ESR1. However, overexpression of ESR2a or ESR2b caused a robust ligand-independent increase in itr2 promoter activity. Deletion analysis of the itr2 promoter indicated that there were novel potential ESR transcription factor-binding sites at −360 bp upstream of the 5′ end of the itr2 promoter. Overall, our study provided novel results regarding the ESRs mediating the onset of parturition in ovoviviparous teleosts.

雌激素可以调节催产素受体的表达，这是通过哺乳动物中的雌激素受体（ESR）介导的，从而启动分娩。为了进一步研究卵胎生硬骨鱼的生殖生理过程，本研究以孔雀鱼（Poecilia reticulata）为研究模型，鉴定ESRs对异产素受体（itrs）的转录调控。由于孔雀鱼胚胎在卵巢内发育，因此在本研究中，对体外用雌二醇（E ₂）处理的怀孕雌性孔雀鱼的卵巢基质中的itr水平进行了测试。E ₂在治疗后3小时仅增加itr2 mRNA水平，而itr1 mRNA表达水平没有变化。在体内实验中，怀孕孔雀鱼浸泡在不同浓度的E _{2中，显着增加了}itr1和itr2在卵巢中的相对表达水平。此外，基于双荧光原位杂交（ISH），esrs和itrs mRNA都定位于卵巢胚胎周围的相同细胞中。为了进一步研究雌激素对itr转录的调节，进行了荧光素酶报告基因测定，结果表明E ₂处理可以诱导ESR1转染细胞中荧光素酶活性的E _{2依赖性抑制。}然而，ESR2a 或 ESR2b 的过度表达引起了itr2启动子活性的强劲不依赖于配体的增加。itr2启动子的缺失分析表明， itr2启动子5'端上游-360 bp处存在新的潜在ESR转录因子结合位点。总的来说，我们的研究提供了关于介导卵胎生硬骨鱼分娩开始的 ESR 的新结果。