Polycomb repression complex 2 is required for the maintenance of retinal progenitor cells and balanced retinal differentiation
Language English Country United States Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
29137925
DOI
10.1016/j.ydbio.2017.11.004
PII: S0012-1606(17)30327-5
Knihovny.cz E-resources
- Keywords
- Differentiation, Eed, Polycomb, Retina,
- MeSH
- Cell Differentiation physiology MeSH
- Chromatin metabolism MeSH
- Enhancer of Zeste Homolog 2 Protein metabolism MeSH
- Histones metabolism MeSH
- Stem Cells cytology metabolism MeSH
- Methylation MeSH
- Mice MeSH
- Neurogenesis MeSH
- Neuroglia metabolism MeSH
- Polycomb Repressive Complex 2 metabolism MeSH
- Cell Proliferation MeSH
- Retina metabolism physiology MeSH
- Animals MeSH
- Check Tag
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Chromatin MeSH
- Eed protein, mouse MeSH Browser
- Ezh2 protein, mouse MeSH Browser
- Enhancer of Zeste Homolog 2 Protein MeSH
- Histones MeSH
- Polycomb Repressive Complex 2 MeSH
Polycomb repressive complexes maintain transcriptional repression of genes encoding crucial developmental regulators through chromatin modification. Here we investigated the role of Polycomb repressive complex 2 (PRC2) in retinal development by inactivating its key components Eed and Ezh2. Conditional deletion of Ezh2 resulted in a partial loss of PRC2 function and accelerated differentiation of Müller glial cells. In contrast, inactivation of Eed led to the ablation of PRC2 function at early postnatal stage. Cell proliferation was reduced and retinal progenitor cells were significantly decreased in this mutant, which subsequently caused depletion of Müller glia, bipolar, and rod photoreceptor cells, primarily generated from postnatal retinal progenitor cells. Interestingly, the proportion of amacrine cells was dramatically increased at postnatal stages in the Eed-deficient retina. In accordance, multiple transcription factors controlling amacrine cell differentiation were upregulated. Furthermore, ChIP-seq analysis showed that these deregulated genes contained bivalent chromatin (H3K27me3+ H3K4me3+). Our results suggest that PRC2 is required for proliferation in order to maintain the retinal progenitor cells at postnatal stages and for retinal differentiation by controlling amacrine cell generation.
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