Figure 2 | Scientific Reports

Figure 2

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

Figure 2

The effect of TCDD on the diurnal rhythmicity of hepatic gene expression in male C57BL/6 mice orally gavaged with sesame oil vehicle or 30 μg/kg TCDD every 4 days for 28 days. (A) The number of hepatic genes which exhibited rhythmic expression in vehicle- and TCDD-treated mice. 5,613 of 5,636 (99.6%) rhythmic genes lost their diurnal oscillation pattern following treatment, while 23 genes exhibited rhythmicity in both vehicle- and TCDD-treated mice. Rhythmicity was determined using JTK_CYCLE (BH q ≤ 0.1). (B) Correlation between the acrophases (time at which cycle peaks/crests) of rhythmic expression in vehicle- and TCDD-treated mice. The linear regression line is shown in green, while the red dashed lines represent acrophase shifts of ± 3 h. Genes falling within the red dashed lines exhibited negligible acrophase shifts of ≤ 1.5 h. TCDD decreased the acrophase of (C) Kpna2 (as well as Polr1b and Max, not shown), while increasing the acrophase of (D) Rorc (as well as Leprotl1, Rtel1, Tef, and Ddo, not shown). Data points represent the average of 3 individual mice ± standard error of the mean. Posterior probabilities (*P1(t) ≥ 0.80) comparing vehicle and TCDD were determined using an empirical Bayes method. Diurnal rhythmicity was assessed using JTK_CYCLE (# BH q ≤ 0.1). Data in (C,D) are double-plotted along the x-axis for better visualization of rhythmicity. (E) Altered amplitudes (fold change) of hepatic genes exhibiting rhythmicity in both vehicle- and TCDD-treated mice. The red dashed line represents a fold change of 1 (i.e. treatment had no effect on amplitude). (F) Genes which lost rhythmicity were compared to previously identified sets of male-specific and liver-specific genes repressed by TCDD56.

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