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Appears in Collections:Aquaculture Journal Articles
Peer Review Status: Refereed
Title: Copper induces Cu-ATPase ATP7A mRNA in a fish cell line, SAF1
Author(s): Minghetti, Matteo
Leaver, Michael
Taggart, John
Casadei, Elisa
Auslander, Meirav
Tom, Moshe
George, Stephen
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Keywords: Copper
Sparus aurata
Issue Date: Aug-2011
Citation: Minghetti M, Leaver M, Taggart J, Casadei E, Auslander M, Tom M & George S (2011) Copper induces Cu-ATPase ATP7A mRNA in a fish cell line, SAF1, Comparative Biochemistry and Physiology - Part C: Toxicology and Pharmacology, 154 (2), pp. 93-99.
Abstract: Copper transporting ATPase, ATP7A, is an ATP dependent copper pump present in all vertebrates, critical for the maintenance of intracellular and whole body copper homeostasis. Effects of copper treatment on ATP7A gene expression in fibroblast cells (SAF1) of the sea bream (Sparus aurata) were investigated by qRT-PCR and by a medium density microarray from a closely related species, striped sea bream (Lithognathus mormyrus). To discriminate between the effects of Cu and other metals, SAF1 cells were exposed to sub-toxic levels of Cu, Zn and Cd. Expression of Cu homeostasis genes copper transporter 1 (CTR1), Cu ATPase (ATP7A), Cu chaperone (ATOX1) and metallothionein (MT) together with the oxidative stress markers glutathione reductase (GR) and Cu/Zn superoxide dismutase (CuZn/SOD) were measured 0, 4 and 24 hours post-exposure by qRT-PCR. Microarray was conducted on samples from 4 hours post Cu exposure. Cu, Zn and Cd increased MT and GR mRNA levels, while only Cu increased ATP7A mRNA levels. Microarray results confirmed the effects of Cu on ATP7A and MT and in addition showed changes in the expression of genes involved in protein transport and secretion. Results suggest that ATP7A may be regulated at the transcriptional level directly by Cu and by a mechanism that is different from that exerteted by metals on MT genes.
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Rights: Published in Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology by Elsevier. This is the peer reviewed version of this article. NOTICE: this is the author’s version of a work that was accepted for publication in Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology, VOL 154, ISSUE 2, (August 2011). DOI: 10.1016/j.cbpc.2011.03.010.

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