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Sci Total Environ. 2019 Jun 15;669:621-630. doi: 10.1016/j.scitotenv.2019.02.440. Epub 2019 Feb 28.

Transcriptomic analysis of Anabas testudineus and its defensive mechanisms in response to persistent organic pollutants exposure.

Author information

1
State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center of Eco-Environment Sciences, Chinese Academy of Sciences, Beijing 100085, China; University of Chinese Academy of Sciences, Beijing 100049, China.
2
China National Genebank-Shenzhen, BGI-Shenzhen, Shenzhen 518083, China; BGI-Qingdao, Qingdao 266510, China.
3
State Environmental Protection Key Laboratory of Dioxin Pollution Control, National Research Center for Environmental Analysis and Measurement, Beijing 100029, China.
4
Woods Hole Oceanographic Institution (WHOI), Woods Hole, MA 02543, USA; Boston University Superfund Research Program, Boston University, Boston, MA 02118, USA.
5
State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center of Eco-Environment Sciences, Chinese Academy of Sciences, Beijing 100085, China; University of Chinese Academy of Sciences, Beijing 100049, China. Electronic address: binzhao@rcees.ac.cn.

Abstract

The freshwater climbing perch (Anabas testudineus) can tolerate water environments contaminated with persistent organic pollutants (POPs). The mechanisms underlying this tolerance are unknown. We used de novo transcriptomic analysis to investigate the defensive mechanisms of A. testudineus against POPs based on its genetic features and biological responses to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure. Our results revealed a specific expansion of cytochrome P450 (CYP) 3A subfamily, which may be involved in the elimination of certain POPs. In xenobiotic responses, the aryl-hydrocarbon receptor (AhR) pathway represents a critical signaling mechanism, and we characterized four AhR and two AhR nuclear translocator homologs and one AhR repressor (AhRR) gene in A. testudineus. TCDD-induced AhRR and CYP1A mRNA upregulation suggests that negative-feedback regulation of AhR signaling through AhRR helps avoid excessive xenobiotic responses. Furthermore, liver and gill transcriptomic profiles were markedly altered after TCDD exposure, with some of the altered genes being related to common defensive responses reported in other species. Based on the newly identified TCDD-altered genes, several A. testudineus-specific responses are proposed, such as enhanced fatty acid β-oxidation. The genetic features of CYP3A subfamily and AhR pathway and the TCDD-induced defensive biological processes elucidated here enhance our understanding of A. testudineus defensive responses against POPs.

KEYWORDS:

Aryl-hydrocarbon receptor; CYP3A; Comparative transcriptomics; Gene family expansion; POPs toxicology; Pollution adaptation

PMID:
30893621
PMCID:
PMC6581032
[Available on 2020-06-15]
DOI:
10.1016/j.scitotenv.2019.02.440
[Indexed for MEDLINE]

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