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Abstract：
Mating in female Drosophila melanogaster causes midgut hypertrophy and reduced lifespan, and these effects are blocked by the drug mifepristone. Eip75B is a transcription factor previously reported to have pleiotropic effects on Drosophila lifespan. Because Eip75B null mutations are lethal, conditional systems and/or partial knock-down are needed to study Eip75B effects in adults. Previous studies showed that Eip75B is required for adult midgut cell proliferation in response to mating. To test the possible role of Eip75B in mediating the lifespan effects of mating and mifepristone, a tripartite FLP-recombinase-based conditional system was employed that provides controls for genetic background. Expression of a Hsp70-FLP transgene was induced in third instar larvae by a brief heat pulse. The FLP recombinase catalyzed the recombination and activation of an Actin5C-GAL4 transgene. The GAL4 transcription factor in turn activated expression of a UAS-Eip75B-RNAi transgene. Inhibition of Eip75B activity was confirmed by loss of midgut hypertrophy upon mating, and the lifespan effects of both mating and mifepristone were eliminated. In addition, the negative effects of mifepristone on egg production were eliminated. The data indicate that Eip75B mediates the effects of mating and mifepristone on female midgut hypertrophy, egg production, and lifespan.
摘要：
雌性果蝇交配会导致中肠肥大和寿命缩短，这些作用被药物米非司酮阻断。Eip75B是先前报道的对果蝇寿命具有多效性作用的转录因子。因为Eip75B无效突变是致命的,需要条件系统和/或部分敲低来研究成人的Eip75B效应。先前的研究表明，Eip75B是成年中肠细胞增殖所必需的。为了测试Eip75B在介导交配和米非司酮的寿命效应中的可能作用，采用了基于三部分FLP重组酶的条件系统，该系统提供了遗传背景的控制。通过短暂的热脉冲在三龄幼虫中诱导Hsp70-FLP转基因的表达。FLP重组酶催化Actin5C-GAL4转基因的重组和活化。GAL4转录因子进而激活UAS-Eip75B-RNAi转基因的表达。通过交配时中肠肥大的丧失证实了Eip75B活性的抑制，并且消除了交配和米非司酮的寿命效应。此外,消除了米非司酮对鸡蛋生产的负面影响。数据表明，Eip75B介导交配和米非司酮对雌性中肠肥大的影响，产蛋,和寿命。
