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Due to recent advancements in molecular methods based on high-throughput DNA sequencing, single cell analytical approaches, and high-resolution microscopy, the time for breaking through these previous limitations has come. We will establish a highly collaborative, innovative team in order to develop the tools necessary to transform our understanding of chromatin architecture and function in mammalian cells. We will begin by developing datasets that establish gold standards for the study of nuclear structure and function using genetic, biochemical and imaging approaches. We will optimize current existing technologies for mapping genome wide chromatin interactions, while also developing novel, complementary approaches for studying chromatin structure. We will also develop innovative analytical methods to interpret the chromatin structural data, unraveling principles of structural- and temporal- chromatin organization. Our highly collaborative team will draw on the diverse experiences of its members to provide a synergistic environment to push the limits of our understanding of nuclear structure. 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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.", "display_title": "Yu M et al. (2024) PMID:39681766", "status": "current", "date_published": "2024-12-16", "@id": "/publications/82acdd68-6f52-41e3-94dd-a926368bd907/", "journal": "Nature structural & molecular biology", "short_attribution": "Yu M et al. 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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. 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