首页> 外文期刊>Aquatic Toxicology >BDE-47 causes developmental retardation with down-regulated expression profiles of ecdysteroid signaling pathway-involved nuclear receptor (NR) genes in the copepod Tigriopus japonicus
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BDE-47 causes developmental retardation with down-regulated expression profiles of ecdysteroid signaling pathway-involved nuclear receptor (NR) genes in the copepod Tigriopus japonicus

机译:BDE-47导致发育迟缓,down足类足癣中蜕皮甾类信号通路相关核受体(NR)基因的表达下调

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2,2',4,4'-Tetrabromodiphenyl ether (BDE-47) is a persistent organic pollutant (POP) in marine environments. Despite its adverse effects (e.g. developmental retardation) in ecdysozoa, the effects of BDE-47 on transcription of ecdysteroid signaling pathway-involved-nuclear receptor (NR) genes and metamorphosis-related genes have not been examined in copepods. To examine the deleterious effect of BDE-47 on copepod molting and metamorphosis, BDE-47 was exposed to the harpacticoid copepod Tigri-opus japonicus, followed by monitoring developmental retardation and transcriptional alteration of NR genes. The developmental rate was significantly inhibited (P 0.05) in response to BDE-47 and the agricultural insecticide gamma-hexachlorocyclohexane. Conversely, the ecdysteroid agonist ponasterone A (PoA) led to decreased molting and metamorphosis time (P 0.05) from the nauplius stage to the adult stage. In particular, expression profiles of all NR genes were the highest at naupliar stages 5-6 except for SVP, FTZ-F1, and HR96 genes. Nuclear receptor USP, HR96, and FTZ-F1 genes also showed significant sex differences (P 0.05) in gene expression levels over different developmental stages, indicating that these genes may be involved in vitellogenesis. NR gene expression patterns showed significant decreases (P 0.05)in response to BDE-47 exposure, implying that molting and metamorphosis retardation is likely associated with NR gene expression. In summary, BDE-47 leads to molting and metamorphosis retardation and suppresses transcription of NR genes. This information will be helpful in understanding the molting and metamorphosis delay mechanism in response to BDE-47 exposure. (C) 2016 Elsevier B.V. All rights reserved.
机译:2,2',4,4'-四溴二苯醚(BDE-47)是海洋环境中的持久性有机污染物(POP)。尽管在蜕皮s中有不利的影响(例如发育迟缓),但尚未在co足类动物中研究过BDE-47对蜕皮甾体信号通路相关的核受体(NR)基因和与变态相关的基因的转录的影响。为了检查BDE-47对co足类蜕皮和变态的有害作用,将BDE-47暴露于类拟co足类Ti足类Tigri-opus japonicus中,然后监测NR基因的发育迟缓和转录改变。响应BDE-47和农用杀虫剂γ-六氯环己烷,显着抑制了发育速度(P <0.05)。相反,蜕皮甾体激动剂ponasterone A(PoA)导致从无节幼体阶段到成年阶段的蜕皮和变态时间减少(P <0.05)。特别是,除了SVP,FTZ-F1和HR96基因外,所有NR基因的表达谱在无节幼体阶段5-6最高。核受体USP,HR96和FTZ-F1基因在不同发育阶段的基因表达水平上也显示出明显的性别差异(P <0.05),表明这些基因可能参与了卵黄发生。 NR基因表达模式显示出对BDE-47暴露的显着降低(P <0.05),这意味着蜕皮和变态延迟可能与NR基因表达有关。总之,BDE-47导致蜕皮和变态发育迟缓,并抑制NR基因的转录。此信息将有助于理解响应BDE-47暴露的蜕皮和变态延迟机制。 (C)2016 Elsevier B.V.保留所有权利。

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