Figure 9. | Epigenomic landscapes of retinal rods and cones

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Epigenomic landscapes of retinal rods and cones

Figure 9.

Affiliation details

Johns Hopkins University School of Medicine, United States; The Salk Institute for Biological Studies, United States; Howard Hughes Medical Institute, The Salk Institute for Biological Studies, United States; Janelia Research Campus, Howard Hughes Medical Institute, United States; University of California San Diego, United States; The University of Western Australia, Australia; Johns Hopkins University, United States
Figure 9.
Download figureOpen in new tabFigure 9. Epigenomic model of rod and cone photoreceptor development.

Enhancers that are active only in progenitor cells (termed 'fetal-only', as the fetal brain was used as a rich source of generic neural progenitors) have low levels of DNA methylation and are enriched for H3K27ac and H3K4me1 histone modifications. In mature cones, histones near fetal-only enhancers lose H3K27ac and H3K4me1 and there is a gain of DNA methylcytosines. In contrast, in mature rods, fetal-only enhancers lose H3K27ac and H3K4me1 but the DNA remains unmethylated, potentially due to the barrier to cytosine methyltransferases posed by their high level of chromatin condensation. In both rods and cones, expressed genes, including rod- and cone-specific photoreceptor genes, have promoters marked by low DNA methylation, high chromatin accessibility, and enrichment for H3K27ac and H3K4me3. Active enhancers are marked by low DNA methylation, high chromatin accessibility, and enrichment for H3K27ac and H3K4me1 (not shown).

DOI: http://dx.doi.org/10.7554/eLife.11613.027