Table 1 Putative dioxin response elements (pDREs) and AhR binding within core clock genes.

From: 2,3,7,8-Tetrachlorodibenzo-p-dioxin abolishes circadian regulation of hepatic metabolic activity in mice

Gene Number of pDREsa Number of AhR Binding Peaksb Max AhR Enrichment Fold Change (AhR vs. IgG) AhR Enrichment at a pDRE? Rhythmicc in VEH? Rhythmicc after TCDD? Phase Shift (h) (TCDD - VEH) Amplitude Fold Change (TCDD vs. VEH)
Arntl 2 4 2.2 No Yes Yes 1.5 −3.9
Clock 10 2 1.9 Yes Yes No N/A N/A
Npas2 14 2 2.3 No Yes Yes 0 −5.2
Nr1d1 1 2 3.2 Yes Yes Yes 1.5 −6.1
Nr1d2 0 3 2.2 No Yes Yes 1.5 −5.3
Rora 9 20 6.5 No No No N/A N/A
Rorc 3 2 2.9 No Yes Yes 6 −9.1
Per1 2 5 2.6 Yes Yes No N/A N/A
Per2 4 7 14.1 Yes Yes Yes −1.5 −4.6
Per3 7 0 N/A No Yes Yes 1.5 −7.2
Cry1 4 1 2.2 No Yes Yes 1.5 −3.8
Cry2 13 4 2.9 Yes Yes No N/A N/A
Nfil3 1 5 3.3 No Yes Yes 0 −3.3
Dbp 3 1 1.9 No Yes Yes 0 −27.3
Tef 5 2 2.0 Yes Yes Yes 4.5 −6.8
Hlf 2 9 7.9 Yes Yes No N/A N/A
  1. aPutative dioxin response elements (pDREs; MSS ≥ 0.856) were identified by computationally querying the mouse genome46.
  2. bAhR genomic enrichment was determined through ChIP-Seq analysis of male livers 2 h after treatment with 30 μg/kg TCDD31.
  3. cRhythmicity was determined using JTK_CYCLE (BH q-value ≤ 0.1; period = 21–24 h)49.