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Freshwater mussels exposed to arsenic and sulfate show contrasting patterns of gene expression
Michalak, P.; Kang, L.; Ciparis, S.; Henley, W.; Jones, J.; Phipps, A.; Hallerman, E. (2016). Freshwater mussels exposed to arsenic and sulfate show contrasting patterns of gene expression, in: Ray, S. (Ed.) Organismal and Molecular Malacology. pp. 99-117. https://dx.doi.org/10.5772/67674
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| Trefwoord |
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| Author keywords |
arsenic, differential gene expression, sulfate, toxicogenomics, transcriptional markers |
| Auteurs | | Top |
- Michalak, P.
- Kang, L.
- Ciparis, S.
- Henley, W.
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- Jones, J.
- Phipps, A.
- Hallerman, E.
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| Abstract |
Freshwater mussels of the Clinch and Powell rivers of Virginia in the southeastern United States have been heavily impacted by runoff, leachates, or spills of materials related to coal extraction, processing, and use. Assays quantifying sublethal impacts of such wastes are needed. We assessed gene transcriptional markers in a laboratory study under controlled conditions, focusing upon arsenic (arsenate, As(V)) and sulphate, contaminants related to coal mining and processing. Pheasantshells Actinonaias pectorosa collected from the Clinch River were subjected to a 28-day chronic exposure to control or environmentally relevant concentrations of each compound. We compared gene expression in digestive gland among parasite-free, female pheasantshells among control and contaminant-exposed individuals using the Illumina HiSeq platform. Statistically significant differential expression of particular genes was observed among control mussels and those exposed to either arsenate or sulfate. Chemical stress was as likely to cause under-expression as it was to cause over-expression of particular genes. Arsenate and sulfate induced up- or down-expression of different suites of 50-100 genes. Our results provide proof-of-principle for using RNAseq technology to approach issues of toxicogenomics in freshwater mussels. The candidate markers could be validated for quantitative PCR assays for rapidly assessing single-gene responses to exposure to toxic compounds. |
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