ArticleEMBO reports2022
The mTORC1-eIF4F axis controls paused pluripotency.
Article in EMBO reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Hyperactivation of mTORC1 blocks stem cell fate transitions through TFE3-NuRD association.EMBO reports · 2026Article
- Emerging roles of ribosome translation in stem cells and stem cell therapy - a review.Cell & bioscience · 2025Review
- The role of serendipity in our investigation of embryo implantation.Developmental biology · 2025Review
- Article
- Unraveling the impact of ZZZ3 on the mTOR/ribosome pathway in human embryonic stem cells homeostasis.Stem cell reports · 2024Article
- A novel regulatory sex-skewing method that inhibits testicular DPY30 expression to increase female rate of dairy goat offspring.Journal of animal science · 2024Article
- Molecular mechanisms of cellular metabolic homeostasis in stem cells.International journal of oral science · 2023Review
- Pausing pluripotency via RNA methylation.Nature cell biology · 2023Article
- A critical role for heme synthesis and succinate in the regulation of pluripotent states transitions.eLife · 2023Article
- Autophagy and pluripotency: self-eating your way to eternal youth.Trends in cell biology · 2022Review
- Review
- The mTORC1-eIF4F axis controls paused pluripotency.EMBO reports · 2022Article
Corrections and comments
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Authors and funding
22 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mouse embryonic stem cells (mESCs) can self-renew indefinitely and maintain pluripotency. Inhibition of mechanistic target of rapamycin (mTOR) by the kinase inhibitor INK128 is known to induce paused pluripotency in mESCs cultured with traditional serum/LIF medium (SL), but the underlying mechanisms remain unclear. In this study, we demonstrate that mTOR complex 1 (mTORC1) but not complex 2 (mTORC2) mediates mTOR inhibition-induced paused pluripotency in cells grown in both SL and 2iL medium (GSK3 and MEK inhibitors and LIF). We also show that mTORC1 regulates self-renewal in both conditions mainly through eIF4F-mediated translation initiation that targets mRNAs of both cytosolic and mitochondrial ribosome subunits. Moreover, inhibition of mitochondrial translation is sufficient to induce paused pluripotency. Interestingly, eIF4F also regulates maintenance of pluripotency in an mTORC1-independent but MEK/ERK-dependent manner in SL, indicating that translation of pluripotency genes is controlled differently in SL and 2iL. Our study reveals a detailed picture of how mTOR governs self-renewal in mESCs and uncovers a context-dependent function of eIF4F in pluripotency regulation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.