ArticleGenes & development2022
Highly rigid H3.1/H3.2-H3K9me3 domains set a barrier for cell fate reprogramming in trophoblast stem cells.
Article in Genes & development, 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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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Gata3 dosage governs primitive endoderm versus trophectoderm specification in embryonic stem cells.EMBO reports · 2026Article
- A de novo H3.2K9me2 deposition pathway establishes heterochromatin for suppressing transposon mobilization during fly somatic development.Nucleic acids research · 2026Article
- Leveraging chorionic villus biopsies for the derivation of patient-specific trophoblast stem cells.Communications biology · 2025Article
- FOXP2 overexpression upregulates LAMA4 expression and thereby alleviates preeclampsia by regulating trophoblast behavior.Communications biology · 2024Article
- Roles of Histone H2B, H3 and H4 Variants in Cancer Development and Prognosis.International journal of molecular sciences · 2024Review
- Conserved and divergent features of trophoblast stem cells.Journal of molecular endocrinology · 2024Review
- Article
- Unreprogrammed H3K9me3 prevents minor zygotic genome activation and lineage commitment in SCNT embryos.Nature communications · 2023Article
- Endogenous retrovirus-derived enhancers confer the transcriptional regulation of human trophoblast syncytialization.Nucleic acids research · 2023Article
- Dynamic antagonism between key repressive pathways maintains the placental epigenome.Nature cell biology · 2023Article
- Suppression of endogenous retroviral enhancers in mouse embryos derived from somatic cell nuclear transfer.Frontiers in genetics · 2022Article
- Similarities and differences in placental development between humans and cynomolgus monkeys.Reproductive medicine and biologyReview
Corrections and comments
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Authors and funding
19 authors at 8 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The placenta is a highly evolved, specialized organ in mammals. It differs from other organs in that it functions only for fetal maintenance during gestation. Therefore, there must be intrinsic mechanisms that guarantee its unique functions. To address this question, we comprehensively analyzed epigenomic features of mouse trophoblast stem cells (TSCs). Our genome-wide, high-throughput analyses revealed that the TSC genome contains large-scale (>1-Mb) rigid heterochromatin architectures with a high degree of histone H3.1/3.2-H3K9me3 accumulation, which we termed TSC-defined highly heterochromatinized domains (THDs). Importantly, depletion of THDs by knockdown of CAF1, an H3.1/3.2 chaperone, resulted in down-regulation of TSC markers, such as
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