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Development

Pausing pluripotency via RNA methylation

Nature Cell Biology volume 25, pages 1241–1242 (2023)Cite this article

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Embryonic diapause in development and paused pluripotency in embryonic stem cells result in a state of hypotranscription through mechanisms that remain unclear. A new study dissects the role of METTL3-deposited global m6A RNA methylation in mediating this transcriptional dormancy.

In around 130 mammal species, the early embryo can enter a dormant developmental state known as embryonic diapause. This phenomenon occurs upon maternal exposure to unfavorable conditions, such as limited food availability or lactation. When conditions become hospitable again, the embryo resumes implantation and development1. Research into the regulation of diapause has revealed that inhibition of the mechanistic target of rapamycin (mTOR) can induce a reversible arrest in both mouse blastocysts and embryonic stem (ES) cells, mimicking the state of embryonic diapause2. mTOR inhibition leads to a reduction in global translation and transcription. This reduction in translation is primarily regulated through the well-established mTOR complex 1 (mTORC1)–eIF4F axis3, but the mechanism by which transcription is regulated during diapause remains unknown. In this issue of Nature Cell Biology, Collignon et al.4 identify a crucial role for mRNA methylation in diapause, exerted by facilitating hypotranscription.

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Fig. 1: m6A modification of mRNA mediates hypotranscription during embryonic diapause.

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  1. Laboratory of Metabolism and Cell Fate, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, China

    Xueting Xu & Baoming Qin

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  1. Xueting Xu
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  2. Baoming Qin
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Correspondence to Baoming Qin.

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The authors declare no competing interests.

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Xu, X., Qin, B. Pausing pluripotency via RNA methylation. Nat Cell Biol 25, 1241–1242 (2023). https://doi.org/10.1038/s41556-023-01203-y

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