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Differential gene expression patterns during embryonic development of sea urchin exposed to triclosan
Author(s) -
Hwang Jinik,
Suh SungSuk,
Park Mirye,
Park So Yun,
Lee Sukchan,
Lee TaekKyun
Publication year - 2017
Publication title -
environmental toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.813
H-Index - 77
eISSN - 1522-7278
pISSN - 1520-4081
DOI - 10.1002/tox.22246
Subject(s) - sea urchin , biology , gene , blastula , paracentrotus lividus , gene expression , embryogenesis , genetics , microbiology and biotechnology , gastrulation
Triclosan (TCS; 2,4,4′‐trichloro‐2′‐hydroxydiphenyl ether) is a broad‐spectrum antibacterial agent used in common industrial, personal care and household products which are eventually rinsed down the drain and discharged with wastewater effluent. It is therefore commonly found in the aquatic environment, leading to the continual exposure of aquatic organisms to TCS and the accumulation of the antimicrobial and its harmful degradation products in their bodies. Toxic effects of TCS on reproductive and developmental progression of some aquatic organisms have been suggested but the underlying molecular mechanisms have not been defined. We investigated the expression patterns of genes involved in the early development of TCS‐treated sea urchin Strongylocentrotus nudus using cDNA microarrays. We observed that the predominant consequence of TCS treatment in this model system was the widespread repression of TCS‐modulated genes. In particular, empty spiracles homeobox 1 (EMX‐1), bone morphogenic protein, and chromosomal binding protein genes showed a significant decrease in expression in response to TCS. These results suggest that TCS can induce abnormal development of sea urchin embryos through the concomitant suppression of a number of genes that are necessary for embryonic differentiation in the blastula stage. Our data provide new insight into the crucial role of genes associated with embryonic development in response to TCS. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 426–433, 2017.