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. 2020 Jul 8;11(9):630–640. doi: 10.1007/s13238-020-00755-1

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© The Author(s) 2020

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Amino acid metabolism in pluripotency regulation. Threonine/methionine metabolism contribute to pluripotency regulation by providing SAM for DNA and histone methylation in PSCs. The threonine dehydrogenase TDH is highly expressed in mESCs, maintaining a high ratio of SAM/SAH that is correlated with high H3K4me3 levels. TDH expression is positively regulated by PRMT5 and negatively regulated by microRNA-9. Metabolism of glutamine and glucose regulates pluripotency through α-KG, which is a cofactor for Jumonji domain-containing histone demethylases (JMDH) and the ten-eleven translocation family of enzymes (TETs) that are involved in DNA demethylation. The cellular level of L-proline is fine-tuned by the amino acid starvation response (AAR) pathway Gcn2-Eif2α-Atf4. Excessive supplementation with L-proline leads to ESC differentiation. Appropriate intracellular synthesis of L-proline safeguards PSC pluripotency