Abstract
Regulation of gene expression by chromatin structure has been under intensive investigation, establishing nuclear organization and genome architecture as a potent and effective means of regulating developmental processes. The substantial growth in our knowledge of the molecular mechanisms underlying retinogenesis has been powered by several genome-wide based tools that mapped chromatin organization at multiple cellular and biochemical levels. Studies profiling the retinal epigenome and transcriptome have allowed the systematic annotation of putative cis-regulatory elements associated with transcriptional programs that drive retinal neural differentiation, laying the groundwork to understand spatiotemporal retinal gene regulation at a mechanistic level. In this review, we outline recent advances in our understanding of the chromatin architecture in the mammalian retina during development and disease. We focus on the emerging roles of non-coding regulatory elements in controlling retinal cell-type specific transcriptional programs, and discuss potential implications in untangling the etiology of eye-related disorders.
Highlights
Specialty section: This article was submitted to Epigenomics and Epigenetics, a section of the journal Frontiers in Genetics
We focus on the emerging roles of non-coding regulatory elements in controlling retinal cell-type specific transcriptional programs, and discuss potential implications in untangling the etiology of eye-related disorders
Genomic studies far have provided insights into modulation of retinal development by chromatin structure, yet the field is still in its infancy and a tremendous amount of work is needed to gain a comprehensive understanding on how epigenetics shape retinal development and are associated with retinal diseases
Summary
The retina has been an excellent system to study neurogenesis, due to its simplified anatomical structure, accessibility and well-defined cell types (Agathocleous and Harris, 2009; Demb and Singer, 2015). The vertebrate mature retina contains seven morphologically and functionally distinct cell types, including six types of neurons (ganglion cells, amacrines, bipolars, horizontal cells, and rod and cone photoreceptors) and one type of glia, the Müller glia (Figure 1) (Cepko et al, 1996). The visual pathway initiates by the response of the photoreceptors to a light stimulus, transducing it into action potentials that propagate to the retinal interneurons (horizontal, bipolar and amacrine cells) and ganglion cells. Retinal differentiation initiates when multipotent retinal progenitor cells (RPCs) exit the cell cycle and differentiate into neurons or glia in a temporally conserved order under the control of gene regulatory networks and signaling pathways (Figure 1) (Wetts and Fraser, 1988; Turner et al, 1990; Agathocleous and Harris, 2009). Mutations in many of these genes underlie severe retinal developmental
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