Department of Biological Sciences, 202 Life Sciences Building, Louisiana State University, Baton Rouge, LA 70803, USA.
Mol Ecol. 2010 Dec;19(23):5186-203. doi: 10.1111/j.1365-294X.2010.04829.x. Epub 2010 Sep 27.
Wild populations of the killifish Fundulus heteroclitus resident in heavily contaminated North American Atlantic coast estuaries have recently and independently evolved dramatic, heritable, and adaptive pollution tolerance. We compared physiological and transcriptome responses to embryonic polychlorinated biphenyl (PCB) exposures between one tolerant population and a nearby sensitive population to gain insight into genomic, physiological and biochemical mechanisms of evolved tolerance in killifish, which are currently unknown. The PCB exposure concentrations at which developmental toxicity emerged, the range of developmental abnormalities exhibited, and global as well as specific gene expression patterns were profoundly different between populations. In the sensitive population, PCB exposures produced dramatic, dose-dependent toxic effects, concurrent with the alterations in the expression of many genes. For example, PCB-mediated cardiovascular system failure was associated with the altered expression of cardiomyocyte genes, consistent with sarcomere mis-assembly. In contrast, genome-wide expression was comparatively refractory to PCB induction in the tolerant population. Tolerance was associated with the global blockade of the aryl hydrocarbon receptor (AHR) signalling pathway, the key mediator of PCB toxicity, in contrast to the strong dose-dependent up-regulation of AHR pathway elements observed in the sensitive population. Altered regulation of signalling pathways that cross-talk with AHR was implicated as one candidate mechanism for the adaptive AHR signalling repression and the pollution tolerance that it affords. In addition to revealing mechanisms of PCB toxicity and tolerance, this study demonstrates the value of comparative transcriptomics to explore molecular mechanisms of stress response and evolved adaptive differences among wild populations.
生活在北美大西洋沿岸受严重污染的河口的丽鱼科鱼类野生种群最近独立地进化出了显著的、可遗传的和适应性的污染耐受能力。我们比较了一个耐受种群和附近敏感种群对胚胎多氯联苯 (PCB) 暴露的生理和转录组反应，以深入了解丽鱼科鱼类进化耐受的基因组、生理和生化机制，这些机制目前尚不清楚。在敏感种群中，PCB 暴露产生了显著的、剂量依赖性的毒性作用，同时伴随着许多基因表达的改变。例如，PCB 介导的心血管系统衰竭与心肌细胞基因表达的改变有关，这与肌节组装错误一致。相比之下，在耐受种群中，全基因组表达对 PCB 的诱导相对不敏感。与敏感种群中观察到的 AHR 途径元件的强烈剂量依赖性上调形成对比的是，耐受与芳烃受体 (AHR) 信号通路的全局阻断有关，AHR 信号通路是 PCB 毒性的关键介质。涉及与 AHR 相互作用的信号通路的改变被认为是 AHR 信号抑制和提供的污染耐受的一种适应性机制的候选机制。本研究不仅揭示了 PCB 毒性和耐受的机制，还展示了比较转录组学在探索野生种群应激反应和进化适应性差异的分子机制方面的价值。
