A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Reference Report

Reference
Citation Céspedes, M.A., Galindo, M.I., Couso, J.P. (2010). Dioxin Toxicity In Vivo Results from an Increase in the Dioxin-Independent Transcriptional Activity of the Aryl Hydrocarbon Receptor.  PLoS ONE 5(11): e15382. (Export to RIS)
FlyBase ID FBrf0212269
Publication Type Research paper
PubMed ID 21079739
PubMed Abstract The Aryl hydrocarbon receptor (Ahr) is the nuclear receptor mediating the toxicity of dioxins--widespread and persistent pollutants whose toxic effects include tumor promotion, teratogenesis, wasting syndrome and chloracne. Elimination of Ahr in mice eliminates dioxin toxicity but also produces adverse effects, some seemingly unrelated to dioxin. Thus the relationship between the toxic and dioxin-independent functions of Ahr is not clear, which hampers understanding and treatment of dioxin toxicity. Here we develop a Drosophila model to show that dioxin actually increases the in vivo dioxin-independent activity of Ahr. This hyperactivation resembles the effects caused by an increase in the amount of its dimerisation partner Ahr nuclear translocator (Arnt) and entails an increased transcriptional potency of Ahr, in addition to the previously described effect on nuclear translocation. Thus the two apparently different functions of Ahr, dioxin-mediated and dioxin-independent, are in fact two different levels (hyperactivated and basal, respectively) of a single function.
DOI 10.1371/journal.pone.0015382
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Language of Publication English
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Publication Type Journal
Abbreviation PLoS ONE
Title PLoS ONE
Publication Year 2006-
ISBN/ISSN 1932-6203
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