status and the presence of NGFI-A (F = 72.71, P < 0.005). Similarly, for the 255-bp promoter construct, there was a significant effect of methylation status (F = 95.18, P < 0.001) and NGFI-A treatment (F = 152.13, P < 0.0005) and a significant interaction between methylation status and the presence of NGFI-A (F = 67.75, P < 0.005). Post hoc testing revealed that, in comparison with the nonmethylated version, patch-methylation inhibited NGFI-A binding to either the 255-bp or 125-bp promoter constructs (P < 0.01; Fig. 4b,c). These findings suggest that the site-selective methylation of the exon 1F NR3C1 promoter construct, mimicking the differences observed between samples obtained from suicide victims with a history of childhood abuse, reduces NGFI-A binding and transcriptional activation through the exon 1F NR3C1 promoter.
