Molecular Biosciences, Northwestern University, Evanston, IL 60208, USA.
Toxicology. 2022 Sep;479:153292. doi: 10.1016/j.tox.2022.153292. Epub 2022 Aug 20.
The genetic variability of toxicant responses among indisviduals in humans and mammalian models requires practically untenable sample sizes to create comprehensive chemical hazard risk evaluations. To address this need, tractable model systems enable reproducible and efficient experimental workflows to collect high-replication measurements of exposure cohorts. Caenorhabditis elegans is a premier toxicology model that has revolutionized our understanding of cellular responses to environmental pollutants and boasts robust genomic resources and high levels of genetic variation across the species. In this study, we performed dose-response analysis across 23 environmental toxicants using eight C. elegans strains representative of species-wide genetic diversity. We observed substantial variation in EC10 estimates and slope parameter estimates of dose-response curves of different strains, demonstrating that genetic background is a significant driver of differential toxicant susceptibility. We also showed that, across all toxicants, at least one C. elegans strain exhibited a significantly different EC10 or slope estimate compared to the reference strain, N2 (PD1074), indicating that population-wide differences among strains are necessary to understand responses to toxicants. Moreover, we quantified the heritability of responses (phenotypic variance attributable to genetic differences between individuals) to each toxicant exposure and observed a correlation between the exposure closest to the species-agnostic EC10 estimate and the exposure that exhibited the most heritable response. At least 20% of the variance in susceptibility to at least one exposure level of each compound was explained by genetic differences among the eight C. elegans strains. Taken together, these results provide robust evidence that heritable genetic variation explains differential susceptibility across an array of environmental pollutants and that genetically diverse C. elegans strains should be deployed to aid high-throughput toxicological screening efforts.
个体之间对毒物反应的遗传变异性在人类和哺乳动物模型中需要实际难以实现的样本量才能进行全面的化学危害风险评估。为了解决这一需求,易于处理的模型系统能够实现可重复且高效的实验工作流程,从而对暴露队列进行高复制测量。秀丽隐杆线虫是一种主要的毒理学模型,它彻底改变了我们对环境污染物引起的细胞反应的理解,并且具有强大的基因组资源和整个物种的高水平遗传变异。在这项研究中,我们使用代表物种广泛遗传多样性的八个秀丽隐杆线虫品系,对 23 种环境毒物进行了剂量反应分析。我们观察到不同品系的剂量-反应曲线的 EC10 估计值和斜率参数估计值存在很大差异,这表明遗传背景是毒物易感性差异的重要驱动因素。我们还表明,在所有毒物中,至少有一种秀丽隐杆线虫品系的 EC10 或斜率估计值与参考品系 N2(PD1074)明显不同,这表明需要在种群范围内比较不同品系之间的差异才能了解对毒物的反应。此外,我们量化了对每种毒物暴露的反应(个体之间遗传差异导致的表型方差)的可遗传性,并观察到与最接近物种无关的 EC10 估计值的暴露和表现出最可遗传反应的暴露之间存在相关性。至少有 20%的每个化合物的至少一个暴露水平的易感性差异可以用这八个秀丽隐杆线虫品系之间的遗传差异来解释。综上所述,这些结果提供了有力的证据,表明可遗传的遗传变异解释了对一系列环境污染物的易感性差异,并且应该部署遗传多样化的秀丽隐杆线虫品系来辅助高通量毒理学筛选工作。