IOCAS-IR  > 实验海洋生物学重点实验室
Molecular phylogenies and evolutionary behavior of AhR (aryl hydrocarbon receptor) pathway genes in aquatic animals: Implications for the toxicology mechanism of some persistent organic pollutants (POPs)
Zhou, Hailong1,2,3,4,5; Qu, Ying1,3,4; Wu, Huifeng1,3; Liao, Chunyang1,3; Zheng, Jiping2; Diao, Xiaoping2; Xue, Qinzhao1,3
2010
发表期刊CHEMOSPHERE
卷号78期号:2页码:193-205
文章类型Review
摘要Phylogenetic analysis of AhR pathway genes and their evolutionary rate variations were studied on aquatic animals. The gene sequences for the proteins involved in this pathway were obtained from four major phylogenetic groups, including bivalvia, amphibian, teleostei and mammalia. These genes were distributed under four major steps of toxicology regulation: formation of cytosolic complex, translocation of AhR, heterodimerization of AhR and induction of CYP1A. The NJ, MP, and ML algorithm were used on protein coding DNA sequences to deduce the evolutionary relationship for the respective AhR pathway gene among different aquatic animals. The rate of non-synonymous nucleotide substitutions per non-synonymous site (d(N)) and synonymous nucleotide substitutions per synonymous site (d(S)) were calculated for different clade of the respective phylogenetic tree for each AhR pathway gene. The phylogenetic analysis suggests that evolutionary pattern of AhR pathway genes in aquatic animals is characterized mainly through gene duplication events or alterative splicing. The d(N) values indicate that all AhR pathway genes are well conserved in aquatic animals, except for CYP1A gene. Furthermore, compare with other aquatic animals, the d(N) value indicates that AhR pathway genes of fish are less conserved, and these genes likely go through an adaptive evolution within aquatic animals. Crown Copyright (C) 2009 Published by Elsevier Ltd. All rights reserved.
关键词Ahr Pathway Non-synonymous Nucleotide Substitutions (d(n)) Synonymous Nucleotide Substitutions (d(s)) Persistent Organic Pollutants (Pops)
DOI10.1016/j.chemosphere.2009.09.012
收录类别SCI
语种英语
WOS记录号WOS:000272888200017
引用统计
被引频次:26[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.qdio.ac.cn/handle/337002/32835
专题实验海洋生物学重点实验室
作者单位1.Chinese Acad Sci, Yantai Inst Coastal Zone Res, Yantai 264003, Shandong, Peoples R China
2.Hainan Univ, Coll Agr, Dept Biotechnol, Haikou 570228, Peoples R China
3.Chinese Acad Sci, Key Lab Coastal Environm Proc, Yantai 264003, Shandong, Peoples R China
4.Chinese Acad Sci, Grad Univ, Beijing 100049, Peoples R China
5.Chinese Acad Sci, Inst Oceanol, Qingdao 266071, Peoples R China
第一作者单位中国科学院海洋研究所
推荐引用方式
GB/T 7714
Zhou, Hailong,Qu, Ying,Wu, Huifeng,et al. Molecular phylogenies and evolutionary behavior of AhR (aryl hydrocarbon receptor) pathway genes in aquatic animals: Implications for the toxicology mechanism of some persistent organic pollutants (POPs)[J]. CHEMOSPHERE,2010,78(2):193-205.
APA Zhou, Hailong.,Qu, Ying.,Wu, Huifeng.,Liao, Chunyang.,Zheng, Jiping.,...&Xue, Qinzhao.(2010).Molecular phylogenies and evolutionary behavior of AhR (aryl hydrocarbon receptor) pathway genes in aquatic animals: Implications for the toxicology mechanism of some persistent organic pollutants (POPs).CHEMOSPHERE,78(2),193-205.
MLA Zhou, Hailong,et al."Molecular phylogenies and evolutionary behavior of AhR (aryl hydrocarbon receptor) pathway genes in aquatic animals: Implications for the toxicology mechanism of some persistent organic pollutants (POPs)".CHEMOSPHERE 78.2(2010):193-205.
条目包含的文件
文件名称/大小 文献类型 版本类型 开放类型 使用许可
Molecular phylogenie(752KB)期刊论文出版稿限制开放ODC PDDL浏览
个性服务
推荐该条目
保存到收藏夹
查看访问统计
导出为Endnote文件
谷歌学术
谷歌学术中相似的文章
[Zhou, Hailong]的文章
[Qu, Ying]的文章
[Wu, Huifeng]的文章
百度学术
百度学术中相似的文章
[Zhou, Hailong]的文章
[Qu, Ying]的文章
[Wu, Huifeng]的文章
必应学术
必应学术中相似的文章
[Zhou, Hailong]的文章
[Qu, Ying]的文章
[Wu, Huifeng]的文章
相关权益政策
暂无数据
收藏/分享
文件名: Molecular phylogenies and evolutionary behavior of AhR (aryl hydrocarbon receptor) pathway genes in aquatic animals_ Implications for the toxicology mechanism of some persistent organic pollutants.pdf
格式: Adobe PDF
所有评论 (0)
暂无评论
 

除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。