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Fig. 1 | Genome Biology

Fig. 1

From: CRISPR/Cas9 offers a new tool for studying the role of chromatin architecture in disease pathogenesis

Fig. 1

Model illustrating the chromatin architectural basis for the aberrant activation of gene expression in prostate cancer. Regions that are associated with prostate cancer risk bind CTCF and interact with each other to maintain the repression of genes within a looped region. Chromatin surrounding the gene is marked by repressive histone H3K27me3. When a prostate cancer risk-associated CTCF anchor region (red arrow becomes red triangle) is deleted by CRISPR/Cas9-based editing, the putative CTCF-mediated loop is no longer formed, and a formerly repressed gene can be accessed and aberrantly activated by an enhancer, marked by H3K27ac, that is located outside the former loop

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Genome Biology

ISSN: 1474-760X

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