Analysing quantitative trait loci of sexual antagonism in fruitflies

进化生物学家长期以来一直对性别之间的差异着迷。雄性和雌性在外观和行为上可能有很大的不同，以绿头鸭为例，两性最初被描述为不同物种的成员。过去的研究表明，两性异形是由于男性和女性生殖角色的不同而产生的。雌性通常会产下大而消耗能量的卵。因此，它们的生殖能力或“健康”受到它们获取资源和生存能力的限制。相比之下，男性产生大量微小而廉价的精子。因此，在大多数情况下，它们的适应性受到吸引配偶的能力的限制，这可能涉及明亮的色彩和奢侈的展示或夸张的武器来保卫高质量的领土。虽然人们理解了性别差异的原因，但男性和女性如何分化的问题尚未解决。潜在的问题是，男性和女性不能独立进化，因为两性通常共享几乎所有的基因。因此，性别之间的任何差异都不是由基因的不同内容引起的，而是依赖于男性和女性使用的不同基因子集。然而，最近的研究结果表明，这种差异化使用基因的进化是不完整的。对从果蝇到鹿等各种生物的研究表明，提高雄性表现的基因组往往会降低雌性表现，反之亦然。这些数据表明，有一些基因以相反的方向影响男性和女性的表现，但在两性中没有差异表达。到目前为止，这些所谓的性拮抗基因只是通过比较同一家族成员的男性和女性的表现（因此可以预期他们共享一部分基因）来间接推断的。我们对引起拮抗作用的基因的身份、它们在生物体中的功能以及它们是如何进化的一无所知。这个项目将填补我们知识上的这一空白。我们将确定对男性和女性表现有相反影响的基因组区域，并确定它们位于何处以及它们包含哪些基因。此外，我们还将研究性对抗在多大程度上可以阻止一种性别中编码高性能的基因在人群中传播，因为它们对另一种性别有负面影响。最后，我们将研究参与拮抗作用的基因座的DNA进化模式，以确定负责性别特异性表现差异的确切核苷酸位点。这样做将使我们能够推断性对抗在这些位点持续了多长时间。通过解决这些多方面的问题，我们的项目将提供信息，帮助我们了解阻止某些基因差异表达的因素。因此，我们将加深我们对男性和女性之间的差异如何演变的一般理解。

Evolutionary biologists have long been fascinated by the differences between the sexes. Males and females can differ profoundly in appearance and behaviour, in the example of the mallard so much so that the sexes were initially described as members of different species. Past research has shown that sexual dimorphism has arisen in response to differing male and female reproductive roles. Females usually produce large and energetically costly eggs. Their reproductive performance, or 'fitness', is therefore limited by their ability to acquire resources and survive. Males, in contrast, produce large amounts of tiny and cheap sperm. Accordingly, their fitness is in most cases limited by their ability to attract mates, which can involve bright colouration and extravagant displays or exaggerated weaponry to defend a territory of high quality. While it is understood why the sexes differ, the question of how males and females diverge has not been resolved. The underlying problem is that males and females cannot evolve independently because the sexes generally share almost all of their genes. Thus, any difference between the sexes is not caused by a different content of genes, but rather relies on a different subset of genes being used in males and females. However, recent results indicate that the evolution of this differential use of genes is incomplete. Studies in a variety of organisms, ranging from fruitflies to deer, have demonstrated that genomes that improve performance in males often tend to decrease performance in females and vice versa. This data indicates that there are genes that affect male and female performance in opposite directions but are not differentially expressed in the two sexes. So far, these so-called sexually antagonistic genes have only been indirectly inferred by comparing the performance of males and females that are members of the same family (and hence can be expected to share a proportion of their genes). Nothing is known about the identity of the genes that cause antagonism, or their function in the organism or how they evolve. This project will fill this gap in our knowledge. We will identify the genomic regions that have opposite effects on male and female performance and determine where they are located and which genes they contain. Further, we will investigate to what extent sexual antagonism can prevent genes that code for high performance in one sex from spreading through the population, due to their negative effect on the other sex. Finally, we will study the patterns of DNA evolution of loci involved in antagonism in order identify the exact nucleotide sites responsible for differences in sex-specific performance. Doing so will allow us to infer for how long sexual antagonism has persisted at these loci. By addressing these multiple aspects, our project will provide information that will help us to understand the factors that prevent some genes from being differentially expressed. Thus we will deepen our general understanding of how differences between males and females can evolve.