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Polycomb repression complex 2 is required for the maintenance of retinal progenitor cells and balanced retinal differentiation
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SYSNO ASEP 0486285 Document Type J - Journal Article R&D Document Type Journal Article Subsidiary J Článek ve WOS Title Polycomb repression complex 2 is required for the maintenance of retinal progenitor cells and balanced retinal differentiation Author(s) Fujimura, Naoko (UMG-J)
Kuželová, Andrea (UMG-J)
Ebert, A. (AT)
Strnad, Hynek (UMG-J) RID
Láchová, Jitka (UMG-J)
Machoň, Ondřej (UMG-J) RID
Busslinger, M. (AT)
Kozmik, Zbyněk (UMG-J) RIDNumber of authors 8 Source Title Developmental Biology. - : Elsevier - ISSN 0012-1606
Roč. 433, č. 1 (2018), s. 47-60Number of pages 14 s. Language eng - English Country US - United States Keywords Retina ; Differentiation ; Polycomb ; Eed Subject RIV EB - Genetics ; Molecular Biology OECD category Biology (theoretical, mathematical, thermal, cryobiology, biological rhythm), Evolutionary biology R&D Projects GA15-23675S GA ČR - Czech Science Foundation (CSF) LQ1604 GA MŠMT - Ministry of Education, Youth and Sports (MEYS) LM2015040 GA MŠMT - Ministry of Education, Youth and Sports (MEYS) ED2.1.00/19.0395 GA MŠMT - Ministry of Education, Youth and Sports (MEYS) Institutional support UMG-J - RVO:68378050 UT WOS 000418394200005 DOI 10.1016/j.ydbio.2017.11.004 Annotation 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 Muller 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 Muller 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. Workplace Institute of Molecular Genetics Contact Nikol Škňouřilová, nikol.sknourilova@img.cas.cz, Tel.: 241 063 217 Year of Publishing 2018
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