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Genetic architecture of susceptibility to PCB126-induced developmental cardiotoxicity in zebrafish.PCB126 诱导斑马鱼发育性心脏毒性易感性的遗传结构。
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3
Genomic mechanisms of evolved physiological plasticity in killifish distributed along an environmental salinity gradient.沿环境盐度梯度分布的食蚊鱼进化生理可塑性的基因组机制。
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4
Mechanistic basis of resistance to PCBs in Atlantic tomcod from the Hudson River.哈德逊河大西洋鲱鱼对多氯联苯的抗性的机制基础。
Science. 2011 Mar 11;331(6022):1322-5. doi: 10.1126/science.1197296. Epub 2011 Feb 17.
5
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Mol Ecol. 2010 Dec;19(23):5186-203. doi: 10.1111/j.1365-294X.2010.04829.x. Epub 2010 Sep 27.
6
Aryl hydrocarbon receptor (AHR)-regulated transcriptomic changes in rats sensitive or resistant to major dioxin toxicities.芳基烃受体(AHR)调节的大鼠对主要二恶英毒性敏感或抗性的转录组变化。
BMC Genomics. 2010 Apr 26;11:263. doi: 10.1186/1471-2164-11-263.
7
Embryonic gene expression among pollutant resistant and sensitive Fundulus heteroclitus populations.污染物抗性和敏感佛罗里达石斑鱼种群的胚胎基因表达。
Aquat Toxicol. 2010 Jul 1;98(3):221-229. doi: 10.1016/j.aquatox.2010.02.022. Epub 2010 Mar 10.
8
2,3,7,8-Tetrachlorodibenzo-p-dioxin upregulates FoxQ1b in zebrafish jaw primordium.2,3,7,8-四氯二苯并对二恶英上调斑马鱼下颚原基中的 FoxQ1b。
Chem Res Toxicol. 2010 Mar 15;23(3):480-7. doi: 10.1021/tx9003165.
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The causes of repeated genetic evolution.重复基因进化的原因。
Dev Biol. 2009 Aug 1;332(1):36-47. doi: 10.1016/j.ydbio.2009.04.040. Epub 2009 May 9.
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Evolutionary mutant models for human disease.人类疾病的进化突变模型。
Trends Genet. 2009 Feb;25(2):74-81. doi: 10.1016/j.tig.2008.11.006. Epub 2008 Dec 26.

极端耐污性的重复进化存在共同的机制。

Common mechanism underlies repeated evolution of extreme pollution tolerance.

机构信息

Department of Biological Sciences, Louisiana State University, 202 Life Sciences Building, Baton Rouge, LA 70803, USA.

出版信息

Proc Biol Sci. 2012 Feb 7;279(1728):427-33. doi: 10.1098/rspb.2011.0847. Epub 2011 Jul 6.

DOI:10.1098/rspb.2011.0847
PMID:21733895
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3234547/
Abstract

Human alterations to the environment can exert strong evolutionary pressures, yet contemporary adaptation to human-mediated stressors is rarely documented in wildlife populations. A common-garden experimental design was coupled with comparative transcriptomics to discover evolved mechanisms enabling three populations of killifish resident in urban estuaries to survive normally lethal pollution exposure during development, and to test whether mechanisms are unique or common across populations. We show that killifish populations from these polluted sites have independently converged on a common adaptive mechanism, despite variation in contaminant profiles among sites. These populations are united by a similarly profound desensitization of aryl-hydrocarbon receptor-mediated transcriptional activation, which is associated with extreme tolerance to the lethal effects of toxic dioxin-like pollutants. The rapid, repeated, heritable and convergent nature of evolved tolerance suggests that ancestral killifish populations harboured genotypes that enabled adaptation to twentieth-century industrial pollutants.

摘要

人类对环境的改变会产生强烈的进化压力,但野生动物种群对人类介导的压力源的适应性变化却很少被记录下来。本研究采用了一种常见的园林实验设计,并结合比较转录组学,来发现使三种生活在城市河口的丽鱼能够在发育过程中正常生存于致死性污染暴露下的进化机制,并检验这些机制在种群间是否是独特的或共同的。我们发现,尽管这些地点的污染物分布不同,但来自这些污染地点的丽鱼种群已经独立地趋同于一种共同的适应性机制。这些种群的共同点是芳烃受体介导的转录激活的敏感性显著降低,这与对有毒二恶英类污染物的致死作用的极端耐受性有关。进化产生的耐受性的快速、重复、可遗传和趋同性质表明,原始的丽鱼种群拥有的基因型使它们能够适应 20 世纪的工业污染物。