Inferring multilayer interactome networks shaping phenotypic plasticity and evolution.
Inferring multilayer interactome networks shaping phenotypic plasticity and evolution.
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DOI：
10.1038/s41467-021-25086-5
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发表时间：
2021-09-06
影响因子：
16.6
通讯作者：
Wu R
中科院分区：
文献类型：
--
作者：
Yang D;Jin Y;He X;Dong A;Wang J;Wu R
表型可塑性代表生物体响应环境刺激而改变其表型的能力。尽管表型可塑性在适应性进化中起着关键作用，但它是如何被遗传控制的仍然是一个谜。在这里，我们开发了一个统一的框架，将全基因组关联研究（GWAS）中的所有单核苷酸多态性（SNP）合并为定量图。该框架集成了功能遗传作图、进化博弈论和捕食者-猎物理论，将每个SNP的净遗传效应分解为独立和依赖的组成部分。独立效应来自SNP的内在能力，仅在其孤立时表达，而依赖效应来自其他SNP的外在影响。依赖效应在概念上超越了上位性的传统定义，它不仅表征了上位性的强度，而且捕捉了上位性的双因果性和因果性的符号。我们实现功能聚类和变量选择推断多层，稀疏，和多重相互作用网络从任何维度的遗传数据。我们使用金黄色葡萄球菌设计并进行了两个GWAS实验，旨在测试该物种对万古霉素暴露和大肠杆菌共存的表型可塑性的遗传机制。我们重建了两个最全面的非生物和生物表型可塑性的遗传网络。通路分析表明，表型可塑性的SNP-SNP上位性可以通过编码基因注释到蛋白质-蛋白质相互作用中。我们的模型可以揭示重要位点的调控机制，挖掘一些不重要位点的缺失遗传力。我们的多层遗传网络提供了一个系统的工具，解剖环境引起的进化。遗传可塑性驱动表型差异。在这里，作者开发了一个框架来量化SNP对感兴趣的表型的个体和组合贡献，并使用它来识别与细菌对外部变化的反应变化相关的SNP-SNP相互作用。
Phenotypic plasticity represents a capacity by which the organism changes its phenotypes in response to environmental stimuli. Despite its pivotal role in adaptive evolution, how phenotypic plasticity is genetically controlled remains elusive. Here, we develop a unified framework for coalescing all single nucleotide polymorphisms (SNPs) from a genome-wide association study (GWAS) into a quantitative graph. This framework integrates functional genetic mapping, evolutionary game theory, and predator-prey theory to decompose the net genetic effect of each SNP into its independent and dependent components. The independent effect arises from the intrinsic capacity of a SNP, only expressed when it is in isolation, whereas the dependent effect results from the extrinsic influence of other SNPs. The dependent effect is conceptually beyond the traditional definition of epistasis by not only characterizing the strength of epistasis but also capturing the bi-causality of epistasis and the sign of the causality. We implement functional clustering and variable selection to infer multilayer, sparse, and multiplex interactome networks from any dimension of genetic data. We design and conduct two GWAS experiments using Staphylococcus aureus, aimed to test the genetic mechanisms underlying the phenotypic plasticity of this species to vancomycin exposure and Escherichia coli coexistence. We reconstruct the two most comprehensive genetic networks for abiotic and biotic phenotypic plasticity. Pathway analysis shows that SNP-SNP epistasis for phenotypic plasticity can be annotated to protein-protein interactions through coding genes. Our model can unveil the regulatory mechanisms of significant loci and excavate missing heritability from some insignificant loci. Our multilayer genetic networks provide a systems tool for dissecting environment-induced evolution. Genetic plasticity drives phenotypic differences. Here, the authors develop a framework to quantify the individual and combinatorial contributions of SNPs on a phenotype of interest and use it to identify SNP-SNP interactions associated with variations in bacteria’s response to external changes.
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影响因子：
6.9
作者：
Diouf I;Derivot L;Koussevitzky S;Carretero Y;Bitton F;Moreau L;Causse M
通讯作者：
Causse M
影响因子：
64.5
作者：
Boyle EA;Li YI;Pritchard JK
通讯作者：
Pritchard JK
影响因子：
3
作者：
Acosta, MBR;Ferreira, RCC;Costa, SOP
通讯作者：
Costa, SOP
影响因子：
5.8
作者：
Bradbury, Peter J.;Zhang, Zhiwu;Buckler, Edward S.
通讯作者：
Buckler, Edward S.
DOI：
10.1007/978-94-007-7347-9_6
发表时间：
2014-01-01
期刊：
ECOLOGICAL GENOMICS: ECOLOGY AND THE EVOLUTION OF GENES AND GENOMES
影响因子：
--
作者：
Abouheif, Ehab;Fave, Marie-Julie;Rajakumar, Rajendhran
通讯作者：
Rajakumar, Rajendhran