ArticleStem cell reports2016
CNOT3-Dependent mRNA Deadenylation Safeguards the Pluripotent State.
Article in Stem cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- The genetic and biochemical determinants of mRNA degradation rates in mammals.Genome biology · 2022Pooled it
- Direct Mapping of CDK2 Substrates in Embryonic Stem Cells Uncovers an AP-Site Repair Mechanism via HMCES Phosphorylation.bioRxiv : the preprint server for biology · 2026Article
- CNOT3 resists ovarian aging by accelerating oocyte maturation and promoting ESCs differentiation.Stem cell research & therapy · 2026Article
- The CCR4-NOT complex: a multifaceted sensor of molecular signals instructing eukaryotic mRNA translation and stability.Nucleic acids research · 2025Review
- Poly(A) tail regulation in stem cells and early development.Cell regeneration (London, England) · 2025Review
- Cnot3 is required for male germ cell development and spermatogonial stem cell maintenance.Development (Cambridge, England) · 2025Article
- mRNA stability fine-tunes gene expression in the developing cortex to control neurogenesis.PLoS biology · 2025Article
- Differences in gene expression between high and low tolerance rainbow trout (Oncorhynchus mykiss) to acute thermal stress.PloS one · 2025Article
- Translation efficiency driven by CNOT3 subunit of the CCR4-NOT complex promotes leukemogenesis.Nature communications · 2024Article
- Clearing the slate: RNA turnover to enable cell state switching?Development (Cambridge, England) · 2023Article
- A unique poly(A) tail profile uncovers the stability and translational activation of TOP transcripts during neuronal differentiation.iScience · 2023Article
- Clinical features of CNOT3-associated neurodevelopmental disorder in three Chinese patients.Neurogenetics · 2023Article
- RNA degradation eliminates developmental transcripts during murine embryonic stem cell differentiation via CAPRIN1-XRN2.Developmental cell · 2022Article
- Cnot8 eliminates naïve regulation networks and is essential for naïve-to-formative pluripotency transition.Nucleic acids research · 2022Article
- RNF219 attenuates global mRNA decay through inhibition of CCR4-NOT complex-mediated deadenylation.Nature communications · 2021Article
- Article
- Molecular Regulation of Paused Pluripotency in Early Mammalian Embryos and Stem Cells.Frontiers in cell and developmental biology · 2021Review
- KLF3 promotes the 8-cell-like transcriptional state in pluripotent stem cells.Cell proliferation · 2020Article
- Decoding pluripotency: Genetic screens to interrogate the acquisition, maintenance, and exit of pluripotency.Wiley interdisciplinary reviews. Systems biology and medicine · 2020Review
- Mass spectrometric identification of candidate RNA-binding proteins associated with Transition Nuclear Protein mRNA in the mouse testis.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
Abstract
Poly(A) tail length and mRNA deadenylation play important roles in gene regulation. However, how they regulate embryonic development and pluripotent cell fate is not fully understood. Here we present evidence that CNOT3-dependent mRNA deadenylation governs the pluripotent state. We show that CNOT3, a component of the Ccr4-Not deadenylase complex, is required for mouse epiblast maintenance. It is highly expressed in blastocysts and its deletion leads to peri-implantation lethality. The epiblast cells in Cnot3 deletion embryos are quickly lost during diapause and fail to outgrow in culture. Mechanistically, CNOT3 C terminus is required for its interaction with the complex and its function in embryonic stem cells (ESCs). Furthermore, Cnot3 deletion results in increases in the poly(A) tail lengths, half-lives, and steady-state levels of differentiation gene mRNAs. The half-lives of CNOT3 target mRNAs are shorter in ESCs and become longer during normal differentiation. Together, we propose that CNOT3 maintains the pluripotent state by promoting differentiation gene mRNA deadenylation and degradation, and we identify poly(A) tail-length regulation as a post-transcriptional mechanism that controls pluripotency.
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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.