Mutations of the zinc finger MYM-type containing 2 (ZMYM2) protein alter cellular and tissue homeostasis, but its functional roles in pluripotency are largely unexplored. Here, I show that ZMYM2 is a key component of the core regulatory network that governs pluripotency. My data reveal that ZMYM2 is a roadblock to efficient somatic cell reprogramming and is required to fine-tune the self-renewal of ESCs and the early differentiation process. Mechanistically, I found that ZMYM2 and LSD1 associate for the transcriptional control of pluripotency and differentiation genes. This study therefore establishes a novel transcriptional regulatory mode dedicated to reprogramming and pluripotency, and open new avenues for exploring the involvement of ZMYM2- LSD1 partnership in development and disease.
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