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Expression profile analysis of antioxidative stress and developmental pathway genes in the manganese-exposed intertidal copepod Tigriopus japonicus with 6K oligochip

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Title
Expression profile analysis of antioxidative stress and developmental pathway genes in the manganese-exposed intertidal copepod Tigriopus japonicus with 6K oligochip
Authors
Kim, Bo-Mi
Choi, Beom-Soon
Lee, Kyun-Woo
Ki, Jang-Seu
Kim, Il-Chan
Choi, Ik-Young
Rhee, Jae-Sung
Lee, Jae-Seong
Subject
Environmental Sciences & Ecology
Keywords
Tigriopus japonicus; Mn; Microarray; Gene expression; Real-time RT-PCR
Issue Date
2013
Citation
Kim, Bo-Mi., et al. 2013. Expression profile analysis of antioxidative stress and developmental pathway genes in the manganese-exposed intertidal copepod Tigriopus japonicus with 6K oligochip. Chemosphere, 92: 1214-1223.
Abstract
Manganese (Mn) provides one of aquatic pollutants in marine ecosystem. Here we used a 6K oligomicroarray to identify the effect of Mn on transcriptomes in the copepod Tigriopus japonicus. A total of 5594 spots were significantly modulated on a 6K oligomicroarray with hierarchical clustering after exposure to Mn over 24 h. Of them, 186 and 489 genes were significantly upregulated and downregulated, respectively. Particularly, several genes involved in stress, detoxification, and developmental functions were significantly modulated in T. japonicus exposed for 24 h. In detail, Mn exposure specifically up-regulated genes that were related to intracellular stress, antioxidant, and detoxification pathways such as cytochrome P450s (CYPs), glutathione S-transferases (GSTs), and heat shock proteins (hsps), while a majority of downregulated genes was associated with developmental pathways such as cuticle protein, ecdysone receptor, and vitellogenin. These results demonstrated that Mn exposure modulated gene expression in relation to intracellular stress, leading to developmental retardation in the intertidal copepod, T. japonicus, and provide a better understanding of mechanistic molecular studies of Mn-induced cellular damage.
DOI
10.1016/j.chemosphere.2013.04.047
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