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. 2009 Sep 16;112(1):245–256. doi: 10.1093/toxsci/kfp191

FIG. 1.

FIG. 1.

Experimental design. Mice harboring either the wild-type AHR (i.e., AHR+/+) or with genetic ablation of the AHR locus (i.e., AHR−/−) in a C57BL/6J background were treated with either corn-oil vehicle (not indicated) or 1000 μg/kg TCDD (i.e., +TCDD). The number of mice used was six in AHR+/+ conditions and three for the AHR−/− conditions. Both liver and kidney were excised 19 h after treatment, RNA extracted, and microarray profiling of mRNA abundances performed as described in “Material and Methods.” General-linear modeling was used to identify three effects. The AHR effect (labeled as “AHR”) gives alterations in mRNA abundance dependent on Ahr genotype, even in the absence of TCDD exposure. The TCDD effect (labeled as “TCDD”) gives alterations in mRNA abundance dependent on TCDD exposure, even in AHR−/− animals. Finally the AHR-TCDD interaction (labeled as “AHR:TCDD”) gives effects dependent on both Ahr genotype and TCDD exposure.