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研究基因复制的结果，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来解释的模式复制的男性偏向的基因在苍蝇。然而，MSCI或表达水平不能解释几个观察结果，包括常染色体对常染色体重复的丰度;某些基因被复制而其他基因不被复制的观察结果，即使所有X连锁管家基因都应该在强大的选择压力下复制;基因重复的持续发生或相同谱系中某些基因重复的复发;或者是在正选择下进化的重复基因的丢失。此外，大多数性拮抗的模型并不包括基因复制，而是提出突变的优势可以解释性别偏见基因的位置。包含基因复制的模型不考虑性拮抗选择从亲本基因开始（即，对于亲本等位基因）和常染色体，并且在异形性染色体和MSCI进化后将继续。介绍了一个基于我们在前一个资助期的结果的创新模型，其中基因复制被认为是产生雄性生殖系功能的重要机制，并提出解决管家基因的基因座内性拮抗冲突（即，选择已经在亲本基因上操作）由组织拮抗作用驱动（即，睾丸拮抗作用）。现在很清楚，由于雄性竞争，分离扭曲和/或寄生虫相关的冲突，睾丸受到强烈的选择，这推动了蛋白质水平和调控区域的快速进化。在这种模式下，基因周转预计也很高。本项目主要研究新基因和亲本基因的功能和拮抗作用，以及睾丸特异性调控区的进化速率和结构。目的1：研究睾丸特异性核转运基因及其亲本基因在雄性生殖系冲突中的功能和作用。目的二是研究新的睾丸特异性基因和亲本线粒体核编码基因变异的拮抗作用。目的3研究受试者特异性调控区的进化速率及其潜在的双向性。敲除、敲低和标记蛋白将用于研究基因的作用、相互作用、细胞定位和共表达。新的基因或亲本基因的变体将异位表达，并将研究对生育力和寿命的影响。全基因组多态性数据来自D.为了实现这些目标，将利用最新的生物信息学工具和分子进化软件对黑腹动物和比较基因组学进行研究。

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.