分子拟态介导的多种基因冲突以及检测这些冲突的计算方法。

IF 6.2 2区 生物学 Q1 CELL BIOLOGY
Shelbi L. Russell , Gabriel Penunuri , Christopher Condon
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引用次数: 0

摘要

在基因组间和自私元素之间的遗传冲突中,驱动元素和杀手元素通过各种分子机制(包括拟态),在敏感元素和目标元素之上实现有偏向的生存、复制或传播。驱动机制体现在生物体的各个层面,从单个基因的偏向传播(如转座元件)到基因组的偏向传播(如病毒),再到细胞系的偏向传播(如癌症)。靶向基因组通过自身信号传递和调控所使用的保守基序,很容易受到分子模仿的影响。模仿这些基调可使基因组间或自私的元素控制核心目标过程,并可发生在序列、结构或功能水平上。分子模拟在二十多年前首次被视为一种重要现象。现代基因组学技术、数据库和机器学习方法为研究分子拟态在自然界遗传冲突中的分布提供了巨大的潜力。在此,我们将探讨冲突基因组间分子拟态的理论预期、已知基因冲突中分子拟态机制的趋势,并概述如何从群体基因组数据集中收集新的实例。我们讨论了涉及短序列图案或基因重复的拟态如何从新突变中趋同进化。而涉及不同结构域或完全折叠结构的过程则是通过水平基因转移在基因组之间发生的。这些趋势主要基于少数生物,应该在一个普遍的、独立于系统发育的框架内重新评估。目前,可从公开数据库中挖掘驱动非孟德尔遗传模式、表观相互作用和趋同蛋白质结构的基因型。这些冲突元素的一个子集可能是分子模拟物。我们提出了从这些数据集中检测遗传冲突和分子模仿的方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Diverse genetic conflicts mediated by molecular mimicry and computational approaches to detect them

In genetic conflicts between intergenomic and selfish elements, driver and killer elements achieve biased survival, replication, or transmission over sensitive and targeted elements through a wide range of molecular mechanisms, including mimicry. Driving mechanisms manifest at all organismal levels, from the biased propagation of individual genes, as demonstrated by transposable elements, to the biased transmission of genomes, as illustrated by viruses, to the biased transmission of cell lineages, as in cancer. Targeted genomes are vulnerable to molecular mimicry through the conserved motifs they use for their own signaling and regulation. Mimicking these motifs enables an intergenomic or selfish element to control core target processes, and can occur at the sequence, structure, or functional level. Molecular mimicry was first appreciated as an important phenomenon more than twenty years ago. Modern genomics technologies, databases, and machine learning approaches offer tremendous potential to study the distribution of molecular mimicry across genetic conflicts in nature. Here, we explore the theoretical expectations for molecular mimicry between conflicting genomes, the trends in molecular mimicry mechanisms across known genetic conflicts, and outline how new examples can be gleaned from population genomic datasets. We discuss how mimics involving short sequence-based motifs or gene duplications can evolve convergently from new mutations. Whereas, processes that involve divergent domains or fully-folded structures occur among genomes by horizontal gene transfer. These trends are largely based on a small number of organisms and should be reevaluated in a general, phylogenetically independent framework. Currently, publicly available databases can be mined for genotypes driving non-Mendelian inheritance patterns, epistatic interactions, and convergent protein structures. A subset of these conflicting elements may be molecular mimics. We propose approaches for detecting genetic conflict and molecular mimicry from these datasets.

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来源期刊
CiteScore
15.10
自引率
1.40%
发文量
310
审稿时长
9.1 weeks
期刊介绍: Seminars in Cell and Developmental Biology is a review journal dedicated to keeping scientists informed of developments in the field of molecular cell and developmental biology, on a topic by topic basis. Each issue is thematic in approach, devoted to an important topic of interest to cell and developmental biologists, focusing on the latest advances and their specific implications. The aim of each issue is to provide a coordinated, readable, and lively review of a selected area, published rapidly to ensure currency.
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