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In mice, imprinted X chromosome inactivation (iXCI) of the paternal X in the pre-implantation embryo and extraembryonic tissues is followed by X reactivation in the inner cell mass (ICM) of the blastocyst to facilitate initiation of random XCI (rXCI) in all embryonic tissues. RNF12 is an E3 ubiquitin ligase that plays a key role in XCI. RNF12 targets pluripotency protein REX1 for degradation to initiate rXCI in embryonic stem cells (ESCs) and loss of the maternal copy of  Rnf12  leads to embryonic lethality due to iXCI failure. Here, we show that loss of  Rex1  rescues the rXCI phenotype observed in  Rnf12   −/−   ESCs, and that REX1 is the prime target of RNF12 in ESCs. Genetic ablation of  Rex1  in  Rnf12   −/−   mice rescues the  Rnf12   −/−   iXCI phenotype, and results in viable and fertile  Rnf12   −/−   :Rex1   −/−   female mice displaying normal iXCI and rXCI. Our results show that REX1 is the critical target of RNF12 in XCI.

REX1 is the critical target of RNF12 in imprinted X chromosome inactivation in mice