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. Author manuscript; available in PMC: 2017 Dec 1.
Published in final edited form as: Mol Psychiatry. 2016 Aug 30;22(12):1746–1758. doi: 10.1038/mp.2016.131

Table 3.

Overlapping dmPFC gene expression changes caused by a history of alcohol dependence (RNA-seq data from PD versus CTL), as well as knockdown of PRDM2 (n = 8–9)

Gene name RNA-seq: PD versus CTL
PRDM2 shRNA versus scramble
H3K9me1 ChIP: PD versus CTL
Fold change P-value Fold change P-value Fold change P-value Region of enrichment
Abcd3   1.27 0.03   −17.5 0.02
Bsn −1.52 0.03 −143.50 0.04 −1.32 0.008 Intron 1/11
−2.21 0.02 Intron 1/11
Cacna1d −1.66 0.02     −5.56 0.01 −1.27 0.005 Intron 8/50
−1.51 0.006 Intron 9/50
Cacna1i −1.71 0.01     −6.75 0.03 −1.27 0.0006 Introns 25/28–27/38
Helz −1.53 0.01     −4.82 0.04
Ncor2 −1.78 0.01     −3.74 0.02
Nop14   1.42 0.02     −8.27 0.01
Rab3c   1.41 0.02     62.73 0.01
Wnk2 −1.99 0.008   −11.55 0.004 −2.06 0.01 Intron 1/26

Abbreviations: ChIP, chromatin immunoprecipitation; CTL, control; dmPFC, dorsomedial prefrontal cortex; H3K9me1, histone 3 at the lysine 9 residue; PD, postdependent; shRNA, short hairpin RNA. Several of these genes may be direct targets of PRDM2, since EdgeR significance analysis of ChIP-seq data identified differential enrichment of H3K9me1 at the indicated genomic loci in the context of alcohol dependence (n = 4).