. 2019 Apr;9(4):a030445. doi: 10.1101/cshperspect.a030445

Table 1.

Overview of the epigenetic machinery

	Writing	Erasing	Reading	Preserving	Remodeling
Histone acetylation	Histone acetyl-transferases (e.g., KAT6B,^a p300/CBP)	Histone deacetylase complexes (e.g., ARID4A,^a HDAC1, HDAC2, HDAC3, HDAC4, HDAC6)	BET bromodomain proteins (e.g., BRD4, BRD2, BRD3)	Unknown	SWI/SNF remodeling complexes (e.g., CHD1,^a CHD3,^a CHD8,^a ARID1A,^a ARID2,^a SMARCA1,^a SMARCAD1,^a ATRX^a)
Histone methylation	Histone methyl-transferases (e.g., KMT2C,^a KMT2D,^a KMT2A,^a SETD2,^a SETDB1,^a EZH2, DOT1L)	Histone demethylases (e.g., KDM6A,^a KDM1A, KDM4B, KDM4C, KDM2A)	Chromodomain, PHD finger proteins	UHRF1, unknown	Mi2-NuRD remodeling complex (CHD3,^a CHD4)
DNA methylation	DNA methyl-transferases (e.g., DNMT1, DNMT3A, DNMT3B)	TET enzymes, BER machinery, and modifiers (e.g., IDH1,^a,b TET1, TET2,^a TET3, TDG)	MBD, zinc finger proteins (e.g., MBD1,^a MBD2, MECP2, ZBTB33)	UHRF1, DNMT1	Variant histones (e.g., H2A.x, H2A.z, H3.3)

Multiple epigenetic machinery proteins have recurrent driver gene mutations in prostate cancer.

^aGenes recurrently harboring driver gene mutations in prostate cancer. Most of the mutations are putative loss-of-function, with the exception of IDH1. Genes that are frequently altered in expression in prostate cancer are shown in italics alone (without superscript).

^bIDH1 is not directly involved in DNA demethylation activity, but recurrent hotspot mutations redirect the activity of IDH1 to generate the metabolite 2-hydroxyglutarate, which can inhibit α-ketoglutarate-dependent oxygenases, including the TET family of enzymes involved in DNA demethylation.