ArticleNature genetics2024
The homeobox transcription factor DUXBL controls exit from totipotency.
Article in Nature genetics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 32 citations in OpenAlex.
- Phase separation of DUX family proteins drives totipotent-like state via 3D genome reorganization and retrotransposon activation.Protein & cell · 2026Article
- Alterations in chromatin organization promote totipotent-like features in a DPPA2/DUX-dependent manner.The EMBO journal · 2026Article
- Mechanisms coordinating exit from the stem cell state in mammals.Genes & development · 2026Review
- The emergence and diversification of the DUX gene family across placental mammals.Communications biology · 2026Article
- Topologically associating domains define the 3D genome architecture of mouse totipotent-like stem cells.The Journal of biological chemistry · 2026Article
- Article
- Coordinated repression of totipotency-associated gene loci by histone methyltransferase EHMT2 via LINE1 regulatory elements.EMBO reports · 2026Article
- Exit from totipotency in mammals: an epigenetic perspective.Frontiers in cell and developmental biology · 2026Review
- CRISPRa-mediated disentanglement of the Dux-MERVL axis in the 2C-like state, totipotency, and cell death.Science advances · 2025Article
- Gene and Genome Duplication in Spiders.Journal of experimental zoology. Part B, Molecular and developmental evolution · 2025Review
- DUX4 at 25: how it emerged from "junk DNA" to become the cause of facioscapulohumeral muscular dystrophy.Skeletal muscle · 2025Review
- Mechanism of cytarabine-induced neurotoxicity.Nature · 2025Article
- Article
- NKX2-5/LHX1 and UHRF1 Establishing a Positive Feedback Regulatory Circuitry Drives Esophageal Squamous Cell Carcinoma through Epigenetic Dysregulation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The ZBTB24-CDCA7-HELLS axis suppresses the totipotent 2C-like reprogramming by maintaining Dux methylation and repression.Nucleic acids research · 2025Article
- The maternal-to-zygotic transition: reprogramming of the cytoplasm and nucleus.Nature reviews. Genetics · 2025Review
- Rise and SINE: roles of transcription factors and retrotransposons in zygotic genome activation.Nature reviews. Molecular cell biology · 2025Article
- Mouse and human embryonic genome activation initiate at the one-cell stage.Frontiers in cell and developmental biology · 2025Article
- The impact of retrotransposons on zygotic genome activation and the chromatin landscape of early embryos.Annals of the New York Academy of Sciences · 2024Review
- Spliceosomal repression: unleashing human cell totipotency.Signal transduction and targeted therapy · 2024Article
Corrections and comments
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Authors and funding
27 authors at 10 institutions in 4 countries.
Funding
Abstract
In mice, exit from the totipotent two-cell (2C) stage embryo requires silencing of the 2C-associated transcriptional program. However, the molecular mechanisms involved in this process remain poorly understood. Here we demonstrate that the 2C-specific transcription factor double homeobox protein (DUX) mediates an essential negative feedback loop by inducing the expression of DUXBL to promote this silencing. We show that DUXBL gains accessibility to DUX-bound regions specifically upon DUX expression. Furthermore, we determine that DUXBL interacts with TRIM24 and TRIM33, members of the TRIM superfamily involved in gene silencing, and colocalizes with them in nuclear foci upon DUX expression. Importantly, DUXBL overexpression impairs 2C-associated transcription, whereas Duxbl inactivation in mouse embryonic stem cells increases DUX-dependent induction of the 2C-transcriptional program. Consequently, DUXBL deficiency in embryos results in sustained expression of 2C-associated transcripts leading to early developmental arrest. Our study identifies DUXBL as an essential regulator of totipotency exit enabling the first divergence of cell fates.
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What OpenQuestion holds
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.