Development of type 2 diabetes following intrauterine growth retardation in rats is associated with progressive epigenetic silencing of Pdx1
J. Clin. Invest. Jun H. Park, et al. 118:2316 doi:10.1172/JCI33655 [Go to this article.]

Figure 3
Histone acetylation and methylation at the Pdx1 promoter. ChIP analysis of cross-linked chromatin from islets of IUGR and control animals at fetal day 21 (A), 2 weeks (B), and 6 months of age (C) IP with antibody to acetylated H3 (AceH3), acetylated H4 (AceH4), H3K4me3, and H3K9me2. Input DNA represents PCR products without prior IP. The IgG IP showed negligible PCR product, indicating little or no IP in the absence of primary antibody. The relative amount of acetylated H3–, acetylated H4–, H3K4me3-, and H3K9me2-bound Pdx1 promoter was measured by Q-PCR and normalized to input DNA. Data are represented as percent of control values. n = 3 experiments, data are ± SEM; *P < 0.05 versus controls.