Skip to main content
. 2021 Jan 12;12:290. doi: 10.1038/s41467-020-20461-0

Fig. 1. Regulation of Slc46a3.

Fig. 1

a Slc46a3 mRNA expression in different mouse tissues after oil (n = 3–4 per group) or TCDD (10 µg/kg for 24 h)(n = 3–4 per group) administration. b Hepatic Slc46a3 mRNA expression after oil (n = 4 per group) or TCDD (10 µg/kg for 24 h)(n = 5 group) administration in Arnt−/− mice. Two-way ANOVA with Bonferroni’s multiple comparisons tests, ***p < 0.0002, ****p < 0.0001. c Male mouse liver transcription profiling by Affymetrix microarray (GEO: GSE55084) shows Slc46a3 mRNA after treatment with PCB-153 (IP injection, 80 mg/kg for 48 h) and TCDD (IP injection, 10 µg/kg for 48 h). Oil (n = 6 per group), PCB-153 (n = 3 per group), TCDD (n = 3 per group). NS not significant. d Putative DRE/XRE binding sites of Slc46a3 promoter were extracted using ChIP-seq data (GEO accession: GSE97634) and possible enhancer region (~ −17,135 bp from the 5′-flanking region of Slc46a3) was analyzed using original file sets using Integrated Genome Browser (Bioviz). e Counting of putative dioxin-responive enhancer (DRE)/xenobiotic response element (XRE) region (−17,135 bp of Slc46a3) binding by AhR after TCDD administration in mouse liver (n = 5 per group). The ChIP-seq data set was from Gene Expression Omnibus (Geo, accession: GSE97634). f Luciferase assay using putative 3×DRE enhancer region (−17,135 bp) of Slc46a3 gene in the Hepa1c1c7 cells. Cells were transfected with 3×DRE or 3×mutDRE luciferase constructs (n = 3 biologically three independent experiments) overnight and treated with indicated doses of TCDD for 6 h. g Inhibitory effect of the AhR inhibitor, CH-223191, on the putative 3×DRE luciferase activity in Hepa1c1c7 cells. After transfection with the 3×DRE luciferase plasmid (n = 3 biologically three independent experiments), cells were co-treated with different concentrations of CH-223191 with/without 10 nM TCDD for 6 h. Transfection was normalized with the Renilla luciferase signal. One-way ANOVA with Tukey’s multiple comparisons test, ****p < 0.0001. h Inhibitory effects of the AhR antagonist CH-223191 on TCDD-induced Slc46a3 mRNA in Hepa1c1c7 cells (n = 5 biologically independent samples). i Expression of hepatic Slc46a3, Cyp1a2, and Ahr mRNAs as a function of mouse age (n=more than 6 per group). One-way ANOVA with Tukey’s multiple comparisons test, ****p < 0.0001. j Expression of hepatic Slc46a3, Cyp1a2, and Ahr mRNAs as a function of time after TCDD treatment (n = 4 per group). One-way ANOVA with Tukey’s multiple comparisons test, ****p < 0.0001. k Expression of Slc46a3 mRNA as a function of dose and time of oil (n = 4 per group) or TCDD (n = 5 per group) treatment. Each data point represents the mean ± SD and adjusted p value, presented in the panels, was determined by unpaired two-tailed Student’s t test using indicated sample sizes and groups.