Nutrient-dependent body size plasticity differs between the sexes in most species, including mammals. Previous work in Drosophila showed that body size plasticity was higher in females, yet the mechanisms underlying increased female body size plasticity remain unclear. Here, we discover that a protein-rich diet augments body size in females and not males because of a female-biased increase in activity of the conserved insulin/insulin-like growth factor signaling pathway (IIS). This sex-biased upregulation of IIS activity was triggered by a diet-induced increase in stunted mRNA in females, and required Drosophila insulin-like peptide 2, illuminating new sex-specific roles for these genes. Importantly, we show that sex determination gene transformer promotes the diet-induced increase in stunted mRNA via transcriptional coactivator Spargel to regulate the male-female difference in body size plasticity. Together, these findings provide vital insight into conserved mechanisms underlying the sex difference in nutrient-dependent body size plasticity.

中文翻译：

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女性偏向的胰岛素途径活性上调介导果蝇体型可塑性的性别差异


在大多数物种（包括哺乳动物）中，依赖于营养的体型可塑性在性别之间存在差异。先前对果蝇的研究表明，雌性体型可塑性较高，但雌性体型可塑性增加的机制仍不清楚。在这里，我们发现富含蛋白质的饮食会增加女性而非男性的体型，因为女性偏向于保守的胰岛素/胰岛素样生长因子信号通路（IIS）的活性增加。这种性别偏向的 IIS 活性上调是由饮食引起的雌性发育不良 mRNA 增加引发的，并且需要果蝇胰岛素样肽 2，阐明了这些基因的新的性别特异性作用。重要的是，我们发现性别决定基因转换器通过转录共激活因子 Spargel 促进饮食诱导的发育不良 mRNA 的增加，从而调节男女体型可塑性的差异。总之，这些发现为营养依赖性体型可塑性性别差异背后的保守机制提供了重要的见解。