Sexual conflict and relocation of genes by duplication

描述(由申请人提供)： 我们研究的长期目标是调查由于基因复制而产生的模式，以更好地了解驱动基因组结构的进化力量。减数分裂性染色体失活(MSCI)、基因表达水平和性拮抗已被提出用来解释果蝇雄性偏向基因的复制模式。然而，MSCI指数或表达水平不能解释几个观察结果，包括常染色体到常染色体重复的丰富；某些基因重复而其他基因不复制，尽管所有X连锁的看家基因都应该处于强烈的选择压力下进行复制；基因重复的持续发生或同一谱系中某些基因的重复重复；或在正选择下进化的重复基因的丢失。此外，大多数性别对抗模型没有包含基因复制，而是提出突变的显性可以解释性别偏见基因的位置。包含基因复制的模型不认为性拮抗选择始于亲本基因(即亲本等位基因)和常染色体，并将在异形性染色体和MSCI进化后继续进行。基于我们在前一个资助时期的结果，引入了一个创新的模型，其中基因复制被认为是产生男性生殖系功能的重要机制，并被提议解决由组织拮抗(即睾丸拮抗)驱动的管家基因(即已在亲本基因上进行的选择操作)的局部内性拮抗冲突。现在很明显，由于男性竞争、分离扭曲和/或与寄生虫相关的冲突，睾丸受到强烈的选择，这正在推动蛋白质水平的快速进化，并可能在调节区。在这种模式下，预计基因周转率也会很高。这个项目有三个目的，研究新基因和亲本基因的功能和拮抗作用，以及睾丸特异调控区的进化速度和结构。目的1研究睾丸特异性核运输基因及其亲本基因在雄性生殖系冲突中的功能和作用。目的2将研究一组新的睾丸特异基因和双亲编码的线粒体基因变异的拮抗作用。目的3研究睾丸特异调控区域的进化速度及其潜在的双向性质。基因敲除、敲除和标记蛋白将用于研究基因的效应、相互作用、细胞定位和共同表达。新的基因或父母基因的变体将以异位方式表达，并将研究其对生育力和寿命的影响。将利用最新的生物信息学工具和分子进化软件来利用来自黑腹毛虫和比较基因组学的全基因组多态数据来实现这些目标。

DESCRIPTION (provided by applicant): The long-term objective of our research is to investigate the patterns that arise as a result of gene duplication to better understand the evolutionary forces that drive genome architecture. Meiotic sex chromosome inactivation (MSCI), the level of gene expression and sexual antagonism have been proposed to explain the patterns of duplication of male-biased genes in flies. However, MSCI or the level of expression cannot account for several observations, including the abundance of autosome-to-autosome duplicates; the observation that certain genes are duplicated while others are not even though all X-linked housekeeping genes should be under strong selective pressure to duplicate; the continued occurrence of gene duplications or the recurrence of duplications of some genes in the same lineage; or the loss of duplicated genes that evolved under positive selection. Additionally, most models of sexual antagonism do not incorporate gene duplication and instead propose that the dominance of the mutations can explain the location of sex-biased genes. Models that incorporate gene duplication do not consider that the sexually antagonistic selection begins with the parental gene (i.e., for parental alleles) and in autosomes and that it will continue after heteromorphic sex chromosomes and MSCI have evolved. An innovative model based on our results from the previous funding period is introduced in which gene duplication is considered to be an important mechanism to generate male germline functions and is proposed to resolve intralocus sexually antagonistic conflicts for housekeeping genes (i.e., selection operating already on the parental gene) driven by tissue antagonism (i.e., testis antagonism). It is now clear that the testes are subject to strong selection due to male competition, segregation distortion and/or parasite-related conflicts, and this is driving rapid evolution at the protein level and likely in regulatory regions. Under this model, gene turnover is also expected to be high. This project has three aims to study the function and antagonistic effects of new genes and parental genes as well as the evolutionary rate and structure of testes-specific regulatory regions. Aim 1 focuses on the function and role of testes-specific nuclear transport genes and their parental genes with respect to male germline conflicts. Aim 2 will investigate the antagonistic effects of a subset of the new testes-specific genes and parental nuclearly encoded mitochondrial gene variations. Aim 3 addresses the study of the rate of evolution of testes-specific regulatory regions and their potential bidirectional nature. Knockouts, knockdowns and tagged proteins will be used to study effects, interactions, cellular localization and co-expression of the genes. New genes or variants of parental genes will be expressed ectopically and the effects on fertility and lifespan will be studied. Whole genome polymorphism data from D. melanogaster and comparative genomics will be exploited using the most current bioinformatics tools and molecular evolution software to achieve these objectives.