The capacity of plants to resist abiotic stresses is of great importance to agricultural, ecological and environmental sustainability, but little is known about its genetic underpinnings. Existing genetic tools can identify individual genetic variants mediating biochemical, physiological, and cellular defenses, but fail to chart an overall genetic atlas behind stress resistance. We view stress response as an eco-evo-devo process by which plants adaptively respond to stress through complex interactions of developmental canalization, phenotypic plasticity, and phenotypic integration. As such, we define and quantify stress response as the developmental change of adaptive traits from stress-free to stress-exposed environments. We integrate composite functional mapping and evolutionary game theory to reconstruct omnigenic, information-flow interaction networks for stress response. Using desert-adapted Euphrates poplar as an example, we infer salt resistance-related genome-wide interactome networks and trace the roadmap of how each SNP acts and interacts with any other possible SNPs to mediate salt resistance. We characterize the previously unknown regulatory mechanisms driving trait variation; i.e., the significance of a SNP may be due to the promotion of positive regulators, whereas the insignificance of a SNP may result from the inhibition of negative regulators. The regulator-regulatee interactions detected are not only experimentally validated by two complementary experiments, but also biologically interpreted by their encoded protein-protein interactions. Our eco-evo-devo model of genetic interactome networks provides an approach to interrogate the genetic architecture of stress response and informs precise gene editing for improving plants’ capacity to live in stress environments.

中文翻译：

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应激反应的生态-进化-进化遗传网络模型

植物抵抗非生物胁迫的能力对农业、生态和环境的可持续性非常重要，但对其遗传基础知之甚少。现有的遗传工具可以识别介导生化、生理和细胞防御的个体遗传变异，但无法绘制出抗逆性背后的整体遗传图谱。我们将胁迫反应视为一个生态进化过程，植物通过发育通道、表型可塑性和表型整合的复杂相互作用来适应性地响应压力。因此，我们将压力反应定义和量化为从无压力环境到有压力环境的适应性特征的发展变化。我们整合复合函数映射和进化博弈论来重构全能，压力反应的信息流交互网络。以适应沙漠的幼发拉底杨树为例，我们推断出与耐盐性相关的全基因组相互作用组网络，并追踪每个 SNP 如何作用并与任何其他可能的 SNP 相互作用以介导耐盐性的路线图。我们描述了以前未知的驱动性状变异的调节机制；即，SNP 的显着性可能是由于正调节因子的促进，而 SNP 的不显着性可能是由于负调节因子的抑制。检测到的调节剂-调节剂相互作用不仅通过两个互补实验进行了实验验证，而且还通过它们编码的蛋白质-蛋白质相互作用进行了生物学解释。