TABLE 2.

Epigenetic factors implicated in naïve and primed hESC control.

Gene name	Function	Effect on naïve or primed hESCs	Epigenetic pathway	References
EZH2	Histone methyltransferase	Required to primed hESCs, but dispensable in naïve hESCs	H3K27me3	Shan et al., 2017
HDAC1/3	Histone deacetylase	Histone deacetylase inhibition was required to establish naïve-like hESCs	Histone deacetylation/transcriptional regulation	Ware et al., 2014
MCRS1, TET1, THAP11	DNA demethylation (TET1) and epigenetic remodeling	Expressed in combination and can convert primed hESCs to naïve-like cells	5mC to 5hmC conversion (TET1) and unknown	Durruthy-Durruthy et al., 2016
NNMT	Nicotinamide N-methyltransferase	Knockout in primed hESCs leads to cells to acquire some naïve characteristics	Reduces histone methylation by removing the methyl-group donor SAM	Sperber et al., 2015
SIRT2	Histone/protein deacetylase	SIRT2 controls primed hESC state	Acetylation and regulation of glycolytic enzymes	Cha et al., 2017
TNKS1/2	Chromatin remodeling	Tankyrase 1/2 inhibition promotes naïve and extended pluripotency	Telomere elongation	Zimmerlin and Zambidis, 2020
TET1/2	DNA demethylation	Required for pluripotency in primed but not the naïve state	5mC to 5hmC conversion	Finley et al., 2018

hESC, human embryonic stem cell; SAM, S-adenosylmethionine.