The Dynamic Epigenetic Landscape of the Retina During Development, Reprogramming, and Tumorigenesis

St. Jude Children's Research Hospital

St. Jude Children's Research Hospital

May 3, 2017

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Visualization of somatic coding and noncoding alterations from ~3,800 pediatric tumors, along with multi-omics information to reveal oncogene activation by noncoding alterations, enhancer hijacking, aberrant splicing, mutual-exclusivity, mutation signature, and more.

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In the developing retina, multipotent neural progenitors undergo unidirectional differentiation in a precise spatiotemporal order. Here we profile the epigenetic and transcriptional changes that occur during retinogenesis in mice and humans. Although some progenitor genes and cell cycle genes were epigenetically silenced during retinogenesis, the most dramatic change was derepression of cell-type-specific differentiation programs. We identified developmental-stage-specific super-enhancers and showed that most epigenetic changes are conserved in humans and mice. To determine how the epigenome changes during tumorigenesis and reprogramming, we performed integrated epigenetic analysis of murine and human retinoblastomas and induced pluripotent stem cells (iPSCs) derived from murine rod photoreceptors. The retinoblastoma epigenome mapped to the developmental stage when retinal progenitors switch from neurogenic to terminal patterns of cell division. The epigenome of retinoblastomas was more similar to that of the normal retina than that of retina-derived iPSCs, and we identified retina-specific epigenetic memory. Paper published in Neuron.  To see additional tracks, click on the 'Tracks' button in the genome browser toolbar. Choose the facet table under FACET. Click on individual cells, assays, or samples to show tracks of interest. 

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