Sexual conflict and relocation of genes by duplication
性冲突和基因复制的重新定位
基本信息
- 批准号:8187321
- 负责人:
- 金额:$ 16.71万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2005
- 资助国家:美国
- 起止时间:2005-05-01 至 2015-04-30
- 项目状态:已结题
- 来源:
- 关键词:AccountingAddressAffectAgreementAllelesArchitectureAutomobile DrivingBioinformaticsCarrier ProteinsChimeric ProteinsComputer softwareConflict (Psychology)DataDrosophila genusEctopic ExpressionEvolutionExcisionFemaleFertilityFertility StudyFundingGene DuplicationGene ExpressionGene ProteinsGenesGeneticGenetic PolymorphismGenomeGenomicsGoalsHousekeeping GeneHyperoxiaImmunityKnock-outLinkLocationLongevityMeasuresMeiosisMitochondriaMitochondrial ProteinsModelingMolecular EvolutionMutationNatureNucleic Acid Regulatory SequencesOvaryParasitesPatternPhosphorusPopulationProductionProteinsRNA InterferenceReactive Oxygen SpeciesRecurrenceReporter GenesResearchResolutionRoleRunningSex BiasSex ChromosomesSex FunctioningStructureSystemTechnologyTestingTestisThinkingTimeTissuesVariantZinc Fingersautosomebasecomparative genomicsdriving forceduplicate genesfitnessflyinnovationinsightmalemutantneuronal cell bodynovelnucleasenucleocytoplasmic transportpressurepromotersegregationsexsite-specific integrationtooltrait
项目摘要
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.
PUBLIC HEALTH RELEVANCE:
In this proposal, we provide an original perspective on topics under intense study, such as patterns of gene duplication, sex-biased expression and the genomic location of sexually antagonistic traits and sexually dimorphic traits. We propose a novel hypothesis describing a new, overlooked role for gene duplication in the resolution of the intralocus sexually antagonistic conflict. The conceptual framework of current thinking on this topic will change if our thesis is supported, as this will imply that new sex-biased duplicate genes are often created from antagonistic alleles of housekeeping genes to resolve sexual antagonism driven by specialization and conflicts in sex-specific tissues.
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,对于父母等位基因)和常染色体,并且在异形性染色体和MSCI进化后它将继续存在。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。目的二是研究一组新的睾丸特异性基因与亲本核编码线粒体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。
公共卫生相关性:
在这项提案中,我们提供了一个原始的角度对正在紧张的研究,如基因复制,性别偏见的表达模式和基因组定位的性拮抗性状和性二态性状的主题。我们提出了一个新的假设,描述了一个新的,被忽视的作用,基因重复的解决intralocus性对抗冲突。如果我们的论点得到支持,当前关于这个主题的思想的概念框架将发生变化,因为这将意味着新的性别偏见重复基因通常是从管家基因的拮抗等位基因中产生的,以解决由性别特异性组织中的专业化和冲突驱动的性拮抗。
项目成果
期刊论文数量(0)
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科研奖励数量(0)
会议论文数量(0)
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{{ truncateString('ESTHER BETRAN', 18)}}的其他基金
Sex chromosomes and relocation of genes by duplication
性染色体和基因复制的重新定位
- 批准号:
7904458 - 财政年份:2009
- 资助金额:
$ 16.71万 - 项目类别:
Sex chromosomes and relocation of genes by duplication
性染色体和基因复制的重新定位
- 批准号:
7221886 - 财政年份:2005
- 资助金额:
$ 16.71万 - 项目类别:
Sex chromosomes and relocation of genes by duplication
性染色体和基因复制的重新定位
- 批准号:
6920428 - 财政年份:2005
- 资助金额:
$ 16.71万 - 项目类别:
Sex chromosomes and relocation of genes by duplication
性染色体和基因复制的重新定位
- 批准号:
7413341 - 财政年份:2005
- 资助金额:
$ 16.71万 - 项目类别:
Sexual conflict and relocation of genes by duplication
性冲突和基因复制的重新定位
- 批准号:
8460170 - 财政年份:2005
- 资助金额:
$ 16.71万 - 项目类别:
Sexual conflict and relocation of genes by duplication
性冲突和基因复制的重新定位
- 批准号:
8324583 - 财政年份:2005
- 资助金额:
$ 16.71万 - 项目类别:
Sex chromosomes and relocation of genes by duplication
性染色体和基因复制的重新定位
- 批准号:
7026997 - 财政年份:2005
- 资助金额:
$ 16.71万 - 项目类别:
Sex chromosomes and relocation of genes by duplication
性染色体和基因复制的重新定位
- 批准号:
7616444 - 财政年份:2005
- 资助金额:
$ 16.71万 - 项目类别:
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