ArticleDevelopment (Cambridge, England)2015
Chd1 is essential for the high transcriptional output and rapid growth of the mouse epiblast.
Article in Development (Cambridge, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 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
62 citing papers in PubMed, 82 citations in OpenAlex.
- Review
- Chromatin remodeling coordinates chromosome compaction, synaptonemal complex architecture and meiotic crossing-over.Research square · 2026Article
- Androgens mediate sexual dimorphism in Pilarowski-Bjornsson syndrome.American journal of human genetics · 2026Article
- A spatial and temporal transcriptomic atlas of mouse intestinal regeneration in the jejunum.Nature communications · 2026Article
- Article
- Spi-1 proto-oncogene regulates mRNA hypertranscription and malignant progression in head and neck cancer.Signal transduction and targeted therapy · 2026Article
- Chromodomain helicase DNA-binding proteins and orofacial cleft.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2026Review
- Epigenetic control of cell identities from epiblast to gastrulation.The FEBS journal · 2025Review
- A direct interaction between the Chd1 CHCT domain and Rtf1 controls Chd1 distribution and nucleosome positioning on active genes.Nucleic acids research · 2025Article
- Emerging roles for the nucleolus in development and stem cells.Development (Cambridge, England) · 2025Review
- 20 years of stemness: From stem cells to hypertranscription and back.Stem cell reports · 2025Review
- Recapitulating and reversing human brain ribosomopathy defects via the maladaptive integrated stress response.Science advances · 2024Article
- Transcriptional repression by a secondary DNA binding surface of DNA topoisomerase I safeguards against hypertranscription.Nature communications · 2023Article
- Myc beyond Cancer: Regulation of Mammalian Tissue Regeneration.Pathophysiology : the official journal of the International Society for Pathophysiology · 2023Review
- ESS2 controls prostate cancer progression through recruitment of chromodomain helicase DNA binding protein 1.Scientific reports · 2023Article
- Review
- HP1 proteins regulate nucleolar structure and function by secluding pericentromeric constitutive heterochromatin.Nucleic acids research · 2023Article
- CHD1, a multifaceted epigenetic remodeler in prostate cancer.Frontiers in oncology · 2023Review
- Superior stemness of a rapidly growing subgroup of isolated human auricular chondrocytes and the potential for use in cartilage regenerative therapy.Regenerative therapy · 2022Article
- Reprogramming of the epigenome in neurodevelopmental disorders.Critical reviews in biochemistry and molecular biology · 2022Review
2 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
The pluripotent mammalian epiblast undergoes unusually fast cell proliferation. This rapid growth is expected to generate a high transcriptional demand, but the underlying mechanisms remain unknown. We show here that the chromatin remodeler Chd1 is required for transcriptional output and development of the mouse epiblast. Chd1(-/-) embryos exhibit proliferation defects and increased apoptosis, are smaller than controls by E5.5 and fail to grow, to become patterned or to gastrulate. Removal of p53 allows progression of Chd1(-/-) mutants only to E7.0-8.0, highlighting the crucial requirement for Chd1 during early post-implantation development. Chd1(-/-) embryonic stem cells (ESCs) have a self-renewal defect and a genome-wide reduction in transcriptional output at both known mRNAs and intergenic transcripts. These transcriptional defects were only uncovered when cell number-normalized approaches were used, and correlate with a lower engagement of RNAP II with transcribed genes in Chd1(-/-) ESCs. We further show that Chd1 directly binds to ribosomal DNA, and that both Chd1(-/-) epiblast cells in vivo and ESCs in vitro express significantly lower levels of ribosomal RNA. In agreement with these findings, mutant cells in vivo and in vitro exhibit smaller and more elongated nucleoli. Thus, the RNA output by both Pol I and II is reduced in Chd1(-/-) cells. Our data indicate that Chd1 promotes a globally elevated transcriptional output required to sustain the distinctly rapid growth of the mouse epiblast.
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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.