ArticleNature structural & molecular biology2025
Integrative analysis of the 3D genome and epigenome in mouse embryonic tissues.
Article in Nature structural & molecular biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Predictive design of tissue-specific mammalian enhancers that function in the mouse embryo.Nature genetics · 2026Article
- Trimodal single-cell profiling of transcriptome, epigenome and 3D genome in complex tissues with scHiCAR.Nature biotechnology · 2026Article
- HiChIA-Rep quantifies the similarity between enrichment-based chromatin interactions datasets.bioRxiv : the preprint server for biology · 2026Article
- Article
- SnapHiC-D: a computational pipeline to identify differential chromatin contacts from single-cell Hi-C data.Briefings in bioinformatics · 2023Article
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Authors and funding
21 authors.
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Abstract
While a rich set of putative cis-regulatory sequences involved in mouse fetal development have been annotated recently on the basis of chromatin accessibility and histone modification patterns, delineating their role in developmentally regulated gene expression continues to be challenging. To fill this gap, here we mapped chromatin contacts between gene promoters and distal sequences across the genome in seven mouse fetal tissues and across six developmental stages of the forebrain. We identified 248,620 long-range chromatin interactions centered at 14,138 protein-coding genes and characterized their tissue-to-tissue variations and developmental dynamics. Integrative analysis of the interactome with previous epigenome and transcriptome datasets from the same tissues revealed a strong correlation between the chromatin contacts and chromatin state at distal enhancers, as well as gene expression patterns at predicted target genes. We predicted target genes of 15,098 candidate enhancers and used them to annotate target genes of homologous candidate enhancers in the human genome that harbor risk variants of human diseases. We present evidence that schizophrenia and other adult disease risk variants are frequently found in fetal enhancers, providing support for the hypothesis of fetal origins of adult diseases.
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