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Nonsense‐mediated  mRNA  decay ( NMD ) is a post‐transcriptional mechanism that targets aberrant transcripts and regulates the cellular  RNA  reservoir. Genetic modulation in vertebrates suggests that  NMD  is critical for cellular and tissue homeostasis, although the underlying mechanism remains elusive. Here, we generate knockout mice lacking Smg6/Est1, a key nuclease in  NMD  and a telomerase cofactor. While the complete loss of Smg6 causes mouse lethality at the blastocyst stage, inducible deletion of Smg6 is compatible with embryonic stem cell ( ESC ) proliferation despite the absence of telomere maintenance and functional  NMD . Differentiation of Smg6‐deficient  ESC s is blocked due to sustained expression of pluripotency genes, normally repressed by  NMD , and forced down‐regulation of one such target, c‐Myc, relieves the differentiation block. Smg6‐null embryonic fibroblasts are viable as well, but are refractory to cellular reprograming into induced pluripotent stem cells ( iPSC s). Finally, depletion of all major  NMD  factors compromises  ESC  differentiation, thus identifying  NMD  as a licensing factor for the switch of cell identity in the process of stem cell differentiation and somatic cell reprograming.

Smg6/Est1 licenses embryonic stem cell differentiation via nonsense‐mediated mRNA decay