ArticleThe EMBO journal2025
TET knockout cells transit between pluripotent states and exhibit precocious germline entry.
Article in The EMBO journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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Who cites it
2 citing papers in PubMed.
- Tet2 modulates ER stress responses related to β-cell death and autoimmunity in diabetes.iScience · 2026Article
- Keeping up with the neighbours: local synchronisation of cell fate decisions during development.EMBO reports · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
TET1, TET2 and TET3 are DNA demethylases with important roles in development and differentiation. To assess the contributions of TET proteins to cell function during early development, single and compound knockouts of Tet genes in mouse pluripotent embryonic stem cells (ESCs) were generated. Here, we show that TET proteins are not required to transit between naïve, formative and primed pluripotency states. Moreover, ESCs with double knockouts of Tet1 and Tet2 or triple knockouts of Tet1, Tet2 and Tet3 are phenotypically indistinguishable. TET1,2,3-deficient ESCs exhibit differentiation defects and fail to activate somatic gene expression, retaining expression of pluripotency transcription factors. Therefore, TET1 and TET2, but not TET3 act redundantly to facilitate somatic differentiation. Importantly however, TET-deficient ESCs can differentiate into primordial germ cell-like cells (PGCLCs), and do so at high efficiency in the presence or absence of PGC-promoting cytokines. Moreover, acquisition of a PGCLC transcriptional programme occurs more rapidly in TET-deficient cells. These results establish that TET proteins act at the juncture between somatic and germline fates: without TET proteins, epiblast cell differentiation defaults to the germline.
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Registered trials
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