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Insights Into the Epigenetics of Retinal Development and Diseases

E. Popova,C. Barnstable

Published 2019 in Epigenetics and Regeneration

ABSTRACT

Abstract The retina is a well-defined and relatively simple part of the central nervous system, and has been studied extensively at both the cellular and molecular level. The transition from stem cell to neuroepithelial progenitor is accompanied by loss of DNA methylation and gains in active epigenetic histone modifications, particularly at genes regulating neuronal fate. Later maturation of progenitor cells is accompanied by a transition to less open chromatin, an increase in heterochromatin and a gain in repressive heterochromatin marks. In the most abundant mouse retinal cell type, the rod photoreceptor, heterochromatin, condenses into a central core of the nucleus occupying about 45% of the volume. Chromatin condensation appears to be a more prevalent method of repressing gene expression than the DNA methylation used by many other cell types. As the rod photoreceptors differentiate, progenitor genes show a shift in histone modifications consistent with gene repression and rod-specific genes develop a signature that consists of increasing levels of H3K4me2 without any H3K27me3. Many retinal diseases are accompanied by changes in the epigenome. The importance of these changes is suggested by the growing numbers of observations showing that manipulating the epigenome can blunt the deleterious effects of mutations or other causes of disease-induced degeneration. As knowledge of the epigenome and ways to manipulate it increases, it is becoming possible to control the differentiation pathways of stem or progenitor cells and thus efficiently produce retinal cells that can be used in regenerative medicine therapies.

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